@article{bertin_frank_breuhaus_schott_kritchevsky_2023, title={Diagnosis and management of thyroid disorders and thyroid hormone supplementation in adult horses and foals}, volume={8}, ISSN={["2042-3306"]}, DOI={10.1111/evj.13981}, abstractNote={Abstract Equine thyroid disorders pose a diagnostic challenge in clinical practice because of the effects of nonthyroidal factors on the hypothalamic–pituitary–thyroid axis, and the horse's ability to tolerate wide fluctuations in thyroid hormone concentrations and survive without a thyroid gland. While benign thyroid tumours are common in older horses, other disorders like primary hypothyroidism or hyperthyroidism in adult horses and congenital hypothyroidism in foals are rare. There is a common misunderstanding regarding hypothyroidism in adult horses, especially when associated with the clinical profile of obesity, lethargy, and poor performance observed in dogs and humans. Low blood thyroid hormone concentrations are often detected in horses as a secondary response to metabolic and disease states, including with the nonthyroidal illness syndrome; however, it is important to note that low thyroid hormone concentrations in these cases do not necessarily indicate hypothyroidism. Assessing equine thyroid function involves measuring thyroid hormone concentrations, including total and free fractions of thyroxine (T4) and triiodothyronine (T3); however, interpreting these results can be challenging due to the pulsatile secretion of thyroid hormones and the many factors that can affect their concentrations. Dynamic testing, such as the thyrotropin‐releasing hormone stimulation test, can help assess the thyroid gland response to stimulation. Although true hypothyroidism is extremely rare, thyroid hormone supplementation is commonly used in equine practice to help manage obesity and poor performance. This review focuses on thyroid gland pathophysiology in adult horses and foals, interpretation of blood thyroid hormone concentrations, and evaluation of horses with thyroid disorders. It also discusses the use of T4 supplementation in equine practice.}, journal={EQUINE VETERINARY JOURNAL}, author={Bertin, Francois-Rene and Frank, Nicholas and Breuhaus, Babetta A. and Schott, Harold C. and Kritchevsky, Janice E.}, year={2023}, month={Aug} }
 @article{fussell_bizikova_breuhaus_harris_moore_chen_linder_2021, title={Bullous amyloidosis in a horse: first description in veterinary medicine}, volume={6}, ISSN={["1365-3164"]}, url={https://doi.org/10.1111/vde.12982}, DOI={10.1111/vde.12982}, abstractNote={Background Bullous amyloidosis is a rare disease in humans that has not been described in a veterinary species in the peer‐reviewed literature. The human disease is characterised by haemorrhagic vesicles and bullae on the skin and mucosae, which form due to amyloid deposition. Hypothesis/Objectives To describe the clinical features, laboratory analysis and histopathological features of an unique presentation of bullous disease in a horse. Animals A 17‐year‐old thoroughbred mare presented for weight loss and severe oral cavity ulcers. Methods and materials Investigations involved haematological evaluation, chemistry profiles, gastroscopy and serum protein electrophoresis, and, postmortem, histopathological evaluation, Congo‐red staining and transmission electron microscopy (TEM). Results Haemorrhagic vesicles and bullae occurred on the mucosa of the oral cavity, lips, oesophagus and stomach, and much less the muzzle, face and mucocutaneous areas of the perineum, where scarring was evident. Histopathological evaluation and Congo‐red staining confirmed the presence of amyloid deposits in dermis and submucosa, in association with vesicle and bulla formation, consistent with bullous amyloidosis. TEM confirmed amyloid fibril deposition in the dermis and along the basement membrane zone. Clefts occurred in the superficial dermis and submucosa, which explained haemorrhage and scarring. The presence of a polyclonal gammopathy and the rapid abolishment of Congo‐red staining with performate pretreatment supported serum amyloid A and secondary amyloidosis. Conclusion and Clinical Importance Bullous amyloidosis is a novel disease of the horse and a newly recognised differential for bullous disease, for which the haemorrhagic nature of bullae, scarring and deep secondary ulcers are considered clinical clues to the condition.}, number={4}, journal={VETERINARY DERMATOLOGY}, publisher={Wiley}, author={Fussell, Devin and Bizikova, Petra and Breuhaus, Babetta and Harris, R. Adam and Moore, A. Russell and Chen, Laura and Linder, Keith E.}, year={2021}, month={Jun} }
 @article{mochizuki_eaton_breuhaus_stowe_2020, title={What is your diagnosis? Transtracheal wash in a horse}, volume={49}, ISSN={["1939-165X"]}, url={https://doi.org/10.1111/vcp.12907}, DOI={10.1111/vcp.12907}, abstractNote={Veterinary Clinical PathologyVolume 49, Issue 4 p. 675-677 WHAT IS YOUR DIAGNOSIS? What is your diagnosis? Transtracheal wash in a horse Hiroyuki Mochizuki, Hiroyuki Mochizuki orcid.org/0000-0002-1520-0393 Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this authorErin Eaton, Erin Eaton Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this authorBabetta Breuhaus, Babetta Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this authorDevorah M. Stowe, Corresponding Author Devorah M. Stowe damarks@ncsu.edu orcid.org/0000-0002-4058-2995 Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA Correspondence Devorah M. Stowe, Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, USA. Email: damarks@ncsu.eduSearch for more papers by this author Hiroyuki Mochizuki, Hiroyuki Mochizuki orcid.org/0000-0002-1520-0393 Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this authorErin Eaton, Erin Eaton Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this authorBabetta Breuhaus, Babetta Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this authorDevorah M. Stowe, Corresponding Author Devorah M. Stowe damarks@ncsu.edu orcid.org/0000-0002-4058-2995 Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA Correspondence Devorah M. Stowe, Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, USA. Email: damarks@ncsu.eduSearch for more papers by this author First published: 21 October 2020 https://doi.org/10.1111/vcp.12907Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume49, Issue4December 2020Pages 675-677 This article also appears in:What is your diagnosis? Virtual Issue RelatedInformation}, number={4}, journal={VETERINARY CLINICAL PATHOLOGY}, publisher={Wiley}, author={Mochizuki, Hiroyuki and Eaton, Erin and Breuhaus, Babetta and Stowe, Devorah M.}, year={2020}, month={Dec}, pages={675–677} }
 @article{breuhaus_2019, title={Glucose and Insulin Responses to an Intravenous Glucose Load in Thoroughbred and Paso Fino Horses}, volume={81}, ISSN={["1542-7412"]}, DOI={10.1016/j.jevs.2019.102793}, abstractNote={Certain breeds of horses may be genetically predisposed to developing insulin dysregulation, which is a risk factor for development of endocrinopathic laminitis in horses. This study was performed to test the hypotheses that Paso Fino horses exhibit evidence of insulin dysregulation compared with Thoroughbred horses and that obesity exaggerates the insulin dysregulation. Intravenous glucose tolerance tests were performed in 14 moderate-weight Thoroughbreds, 12 moderate-weight Paso Finos, and 12 overweight Paso Finos. Moderate Paso Finos had greater baseline serum insulin concentrations, area under the insulin concentration curve, peak insulin, insulin-to-glucose ratio, area under the insulin to glucose curve, and modified glucose-to-insulin ratio compared with moderate Thoroughbreds. The reciprocal inverse square of basal insulin (RISQI) and glucose-to-insulin ratio were significantly lower in moderate Paso Finos compared with moderate Thoroughbreds. Overweight Paso Finos had greater baseline insulin concentrations, area under the insulin concentration curve, time to peak insulin, baseline plasma glucose concentration, insulin-to-glucose ratio, and area under the insulin to glucose curve compared with moderate Paso Finos. The RISQI and glucose-to-insulin ratio were significantly lower in overweight Paso Finos compared with moderate Paso Finos. In conclusion, moderate-weight Paso Finos had higher baseline serum insulin concentrations and an excessive hyperinsulinemic response to an intravenous glucose load when compared with moderate-weight Thoroughbreds. Overweight Paso Finos had even greater baseline insulin concentrations and hyperinsulinemic responses to glucose compared with moderate Paso Finos, as well as greater baseline plasma glucose concentrations. Paso Finos exhibit insulin dysregulation compared with Thoroughbreds.}, journal={JOURNAL OF EQUINE VETERINARY SCIENCE}, author={Breuhaus, Babetta A.}, year={2019}, month={Oct} }
 @article{breuhaus_2019, title={Thyroid Hormone and Thyrotropin Concentrations and Responses to Thyrotropin-Stimulating Hormone in Horses with PPID Compared with Age-Matched Normal Horses}, volume={75}, ISSN={["1542-7412"]}, DOI={10.1016/j.jevs.2019.01.008}, abstractNote={Glucocorticoids are known to exert inhibitory action on the hypothalamic-pituitary-thyroid axis. With recent evidence that free plasma cortisol and urinary excretion of cortisol metabolites may be increased in horses with pituitary pars intermedia dysfunction (PPID), it is important to further examine thyroid function in horses with PPID. To test the hypothesis that serum thyrotropin (TSH) concentrations are decreased in horses with PPID, baseline serum thyroid hormone and TSH concentrations, and responses to TSH-releasing hormone (TRH), were compared between 12 horses diagnosed as having PPID and 14 age-matched normal horses. Horses with PPID had resting serum concentrations of free thyroxine by equilibrium dialysis (fT4D) and TSH that were significantly lower than serum concentrations of fT4D and TSH in age-matched normal horses. Serum concentrations of total T4 and total and free triiodothyronine (T3) were also lower in horses with PPID compared with normal horses, but the differences did not reach statistical significance. Thyroid hormone and TSH responses to TRH administration were not different between horses with PPID and normal horses. In conclusion, serum fT4D concentrations are decreased in horses with PPID without an appropriate increase in serum TSH concentrations. Normal serum thyroid hormone and TSH concentration responses to exogenous TRH administration support the theory that increased glucocorticoid activity in horses with PPID may exert prolonged tonic suppression, but not complete inhibition, of TRH and subsequent TSH release, similar to what has been observed in other species.}, journal={JOURNAL OF EQUINE VETERINARY SCIENCE}, author={Breuhaus, Babetta A.}, year={2019}, month={Apr}, pages={35–40} }
 @article{linder_bizikova_luff_zhou_yuan_breuhaus_nelson_mackay_2018, title={Generalized papillomatosis in three horses associated with a novel equine papillomavirus (EcPV8)}, volume={29}, number={1}, journal={Veterinary Dermatology}, author={Linder, K. E. and Bizikova, P. and Luff, J. and Zhou, D. and Yuan, H. and Breuhaus, B. and Nelson, E. and Mackay, R.}, year={2018} }
 @article{breuhaus_2018, title={Serum Thyroid Hormone and Thyrotropin Concentrations in Adult Horses as They Age}, volume={68}, ISSN={["1542-7412"]}, DOI={10.1016/j.jevs.2018.04.006}, abstractNote={With more horses remaining active longer in life, it is important to characterize changes that occur normally with aging, so that these can be differentiated from development of disease. The objective of the study was to test the hypotheses that geriatric horses have lower circulating concentrations of thyroid hormones and/or higher serum thyrotropin (TSH) concentrations compared to younger horses. Serum thyroid hormone and TSH concentrations from 71 normal, healthy horses that had participated in prior research projects were analyzed for effects of age, sex, and season when samples were obtained. All samples had been assayed in the same previously validated radioimmunoassays. There were no differences in serum concentrations of thyroid hormones or TSH by sex or season. Serum total thyroxine (T4) was greater in 3- to 6-year-old horses compared to all other age groups and was negatively correlated with age. There were no differences among age groups for free T4 and total and free tri-iodothyronine (T3). Serum TSH concentration was significantly greater in old horses (≥15 or ≥20 years) compared to young (3–10 years) and intermediate (11–14 years) age groups. Serum TSH was positively correlated with age. There were no significant differences in thyroid hormone responses to thyrotropin releasing hormone (TRH) among young, intermediate, or old horses. However, the TSH response to TRH was significantly different in both groups of older horses compared to intermediate and young horses. Serum total thyroxine concentrations decrease and serum TSH concentrations increase in horses as they age, with no changes in free T4 or T3.}, journal={JOURNAL OF EQUINE VETERINARY SCIENCE}, author={Breuhaus, Babetta A.}, year={2018}, month={Sep}, pages={21–25} }
 @article{saetra_breuhaus_hildebran_2018, title={Unilateral nephrolithiasis with renal rupture in a horse}, volume={30}, ISSN={["2042-3292"]}, DOI={10.1111/eve.12756}, abstractNote={Summary A 22‐year‐old Thoroughbred mare presented to North Carolina State University Large Animal Hospital for evaluation of acute colic. After initial work‐up, the mare was diagnosed and treated for presumed gas colic. She was subsequently further diagnosed and treated for gastric ulcers and mild sand accumulation in her large colon, based on gastroscopy and abdominal radiographs, respectively. The mare initially responded well to medical management of colic, but on Day 3 of hospitalisation, developed a low grade fever and signs of mild discomfort returned. Abdominocentesis at that time revealed an aseptic peritonitis and she was placed on antibiotics and NSAID s. When no significant improvement was achieved, the mare was taken to surgery 2 days later. In surgery, she was diagnosed with nephrolithiasis of the left kidney that had erupted through the renal capsule and into the retroperitoneal space, as well as into the abdomen. Two nephroliths were found in the omentum. The mare was subjected to euthanasia due to a poor prognosis and submitted for necropsy, where 54 nephroliths were identified, associated with the left kidney. This report describes significant unilateral nephrolithiasis (to the point of renal rupture) in a horse with no azotaemia or other clinical signs of urinary tract disease.}, number={12}, journal={EQUINE VETERINARY EDUCATION}, author={Saetra, T. and Breuhaus, B. and Hildebran, A.}, year={2018}, month={Dec}, pages={635–639} }
 @article{meichner_kraszeski_durrant_grindem_breuhaus_moore_neel_linder_borst_fogle_et al._2016, title={Extreme lymphocytosis with myelomonocytic morphology in a horse with diffuse large B-cell lymphoma}, volume={46}, ISSN={0275-6382}, url={http://dx.doi.org/10.1111/vcp.12435}, DOI={10.1111/vcp.12435}, abstractNote={An 11-year-old, 443-kg Haflinger mare was presented to the North Carolina State University Veterinary Teaching Hospital with a 2-week history of lethargy and a 3-day duration of anorexia, pyrexia, tachycardia, and ventral edema. Severe pitting edema, peripheral lymphadenopathy, and a caudal abdominal mass were noted on physical examination. An extreme leukocytosis (154.3 × 103 /μL) and microscopic hematologic findings suggestive of myelomonocytic leukemia were observed. Serum protein electrophoresis revealed a monoclonal gammopathy and urine protein electrophoresis revealed a monoclonal light chain proteinuria. Necropsy and histopathology confirmed widespread neoplastic infiltration in many organs with a heterogenous population of cells; there was no apparent evidence of bone marrow involvement. Immunohistochemistry confirmed presence of a majority of B cells with a limited antigen expression, admixed with a lower number of T cells. Molecular clonality analysis of IgH2, IgH3, and kappa-deleting element (KDE, B cell) on whole blood and KDE on infiltrated tissues revealed clonal rearrangements, and the KDE intron clones that amplified in blood and in infiltrated tissue were identical. In contrast, the clonality analysis of T-cell receptor γ revealed no clonality on blood cells and infiltrated tissues. In conjunction with the histopathologic changes, the lesion was interpreted to be composed of neoplastic B cells with a reactive T-cell population. Polymerase chain reaction testing for equine herpes virus 5 was negative. The final diagnosis was diffuse large B-cell lymphoma with a marked hematogenous component.}, number={1}, journal={Veterinary Clinical Pathology}, publisher={Wiley}, author={Meichner, Kristina and Kraszeski, Blaire H. and Durrant, Jessica R. and Grindem, Carol B. and Breuhaus, Babetta A. and Moore, Peter F. and Neel, Jennifer A. and Linder, Keith E. and Borst, Luke B. and Fogle, Jonathan E. and et al.}, year={2016}, month={Dec}, pages={64–71} }
 @inbook{breuhaus_2015, place={St Louis, MO}, edition={5th}, title={Anhidrosis}, booktitle={Large animal internal medicine}, publisher={Mosby Elsevier}, author={Breuhaus, B.A.}, editor={Smith, B.P.Editor}, year={2015}, pages={1233–1236} }
 @inbook{breuhaus_2015, place={St. Louis, MO}, edition={5th edition}, title={Thyroid glands}, booktitle={Large animal internal medicine}, publisher={Mosby Elsevier}, author={Breuhaus, B.A.}, editor={Smith, B.P.Editor}, year={2015}, pages={1236–1240} }
 @article{pemberton_choi_mayer_li_gokey_svaren_safra_bannasch_sullivan_breuhaus_et al._2014, title={A Mutation in the Canine Gene Encoding Folliculin-Interacting Protein 2 (FNIP2) Associated With a Unique Disruption in Spinal Cord Myelination}, volume={62}, ISSN={["1098-1136"]}, DOI={10.1002/glia.22582}, abstractNote={Novel mutations in myelin and myelin-associated genes have provided important information on oligodendrocytes and myelin and the effects of their disruption on the normal developmental process of myelination of the central nervous system (CNS). We report here a mutation in the folliculin-interacting protein 2 (FNIP2) gene in the Weimaraner dog that results in hypomyelination of the brain and a tract-specific myelin defect in the spinal cord. This myelination disruption results in a notable tremor syndrome from which affected dogs recover with time. In the peripheral tracts of the lateral and ventral columns of the spinal cord, there is a lack of mature oligodendrocytes. A genome-wide association study of DNA from three groups of dogs mapped the gene to canine chromosome 15. Sequencing of all the genes in the candidate region identified a frameshift mutation in the FNIP2 gene that segregated with the phenotype. While the functional role of FNIP2 is not known, our data would suggest that production of truncated protein results in a delay or failure of maturation of a subpopulation of oligodendrocytes.}, number={1}, journal={GLIA}, author={Pemberton, Trevor J. and Choi, Sunju and Mayer, Joshua A. and Li, Fang-Yuan and Gokey, Nolan and Svaren, John and Safra, Noa and Bannasch, Danika L. and Sullivan, Katrina and Breuhaus, Babetta and et al.}, year={2014}, month={Jan}, pages={39–51} }
 @article{davis_kruger_lafevers_barlow_schirmer_breuhaus_2014, title={Effects of quinapril on angiotensin converting enzyme and plasma renin activity as well as pharmacokinetic parameters of quinapril and its active metabolite, quinaprilat, after intravenous and oral administration to mature horses}, volume={46}, ISSN={["2042-3306"]}, DOI={10.1111/evj.12206}, abstractNote={Summary Reasons for performing study Angiotensin converting enzyme ( ACE ) inhibitors improve survival and quality of life in human patients and small animals with cardiovascular and renal disease. There is limited information regarding their effects in horses. Objectives The purpose of this study was to determine the pharmacokinetics of quinapril and its effects on ACE and renin in horses. Study design Experimental study using healthy mature horses. Methods Six healthy horses were administered quinapril at 120 mg i.v., 120 mg per os and 240 mg per os in a 3‐way crossover design. Blood was collected for measurement of quinapril and quinaprilat concentrations using ultra‐high pressure liquid chromatography with mass spectrometry. Angiotensin converting enzyme activity and renin activity were measured using a radioenzymatic assay. Noncompartmental pharmacokinetic modelling and statistical analyses were performed. Results No adverse effects were observed during the study period. Intravenous and oral administration significantly inhibited ACE activity. Renin concentrations increased in all groups, but this increase was not statistically significant. Following i.v. administration of quinapril, mean terminal half‐life was 0.694 h and 1.734 h for quinapril and quinaprilat, respectively. The mean volume of distribution and clearance for quinapril were 0.242 l/kg bwt and 11.93 ml/kg bwt/min, respectively. Maximum concentration for quinaprilat was 145 ng/ml at 0.167 h. Bioavailability of quinapril following oral administration was <5%. Quinaprilat was detected in all horses following oral administration of quinapril; however, it was below the limit of quantification of the assay (2.5 ng/ml) for most horses in the 120 mg dosing group. Conclusions These results suggest that, despite low plasma concentrations, quinapril has sufficient oral absorption to produce inhibition of ACE in healthy horses. Controlled studies in clinically affected horses are indicated. Quinapril provides a potential treatment alternative for horses with cardiovascular and renal disease.}, number={6}, journal={EQUINE VETERINARY JOURNAL}, author={Davis, J. L. and Kruger, K. and LaFevers, D. H. and Barlow, B. M. and Schirmer, J. M. and Breuhaus, B. A.}, year={2014}, month={Nov}, pages={729–733} }
 @article{hildebran_breuhaus_refsal_2014, title={Non-thyroidal-Illness-syndrome in adult horses}, volume={30}, number={6}, journal={Pferdeheilkunde}, author={Hildebran, A. C. and Breuhaus, B. A. and Refsal, K. R.}, year={2014}, pages={729–730} }
 @article{hilderbran_breuhaus_refsal_2014, title={Nonthyroidal Illness Syndrome in Adult Horses}, volume={28}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.12274}, abstractNote={Background This study was performed to determine whether sick horses have thyroid hormone ( TH ) alterations similar to those observed in nonthyroidal illness syndrome in other species. Hypothesis Horses suffering from systemic diseases have decreased TH s and inappropriately low thyroid‐stimulating hormone ( TSH ). Animals Seventy‐one clinically normal horses; 380 hospitalized horses. Methods Total thyroxine ( TT 4), free thyroxine by equilibrium dialysis ( fT 4D), total triiodothyronine ( TT 3), free triiodothyronine ( fT 3), and TSH were measured in normal and hospitalized horses. Disease severity was categorized as mild, moderate, or severe by both subjective and objective criteria. Results Negative correlations existed between all TH s, except TSH , and objective illness severity scores. These scores also increased with each subjective disease severity category. TT 3 and fT 3 were decreased with mild disease. TT 3 progressively decreased more with moderate and severe disease. TT 4 and fT 4D remained normal with mild disease, but decreased progressively with disease severity. TSH increased with mild disease, but remained normal with moderate or severe disease. Horses that died or were euthanized had lower concentrations of all TH s, except TSH , when compared with those that lived. In horses that received >3 doses of NSAIDs, corticosteroids, or heparin compared to 0–3 doses, TT 3 and TT 4 were decreased, whereas fT 4D and TSH remained normal. There were minimal TH changes in horses that were not eating. Conclusions and Clinical Importance Thyroid hormones decrease in horses with systemic disease. TT 3 decreases first, followed by TT 4 and fT 4D. TSH fails to increase proportionally to the changes in TH s, indicating hypothalamic–pituitary axis dysregulation. NSAIDs, corticosteroids, heparin, and fasting have less effect on TH s compared with disease severity.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Hilderbran, A. C. and Breuhaus, B. A. and Refsal, K. R.}, year={2014}, month={Mar}, pages={609–617} }
 @article{breuhaus_2014, title={Thyroid Function and Dysfunction in Term and Premature Equine Neonates}, volume={28}, ISSN={["1939-1676"]}, DOI={10.1111/jvim.12382}, abstractNote={Background This study was performed to compare thyroid function of premature foals to term foals. Hypothesis Premature foals are more markedly hypothyroxinemic than expected for their severity of illness alone. Animals Twenty clinically normal term foals; 28 sick, hospitalized term foals; 24 sick, hospitalized premature foals. Methods Thyroid hormones ( TH ) and thyrotropin ( TSH ) were measured, both at rest and in response to thyrotropin‐releasing hormone ( TRH ), in the 3 groups of foals. Clinical and clinicopathologic data were recorded. Results Normal foals had high TH at birth, which decreased over the first month into the normal reference range for adult horses. TSH was within the normal adult reference range soon after birth, and did not change over time. At 24–36 hours of age, triiodothyronine (T3) was significantly lower in both premature and term hospitalized foals compared to normal foals; premature foals were not different from term hospitalized foals. Thyroxine (T4) was not different between normal and term hospitalized foals, but was significantly lower than in premature foals of both of these groups. TSH was not different among the 3 groups. TRH stimulation tests identified significant differences in T4 among all 3 groups of foals, whereas T3 was similar in premature and term hospitalized foals and different from normal foals. TSH response to TRH was significantly higher in premature foals compared to normal foals. Conclusions and Clinical Importance The hypothalamic‐pituitary‐thyroid axis is different in foals compared to adult horses. Sick foals exhibit nonthyroidal illness syndrome. Premature foals are more markedly hypothyroxinemic than can be accounted for by their severity of illness alone.}, number={4}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Breuhaus, B. A.}, year={2014}, pages={1301–1309} }
 @article{jennings_wise_nickeleit_maes_cianciolo_piero_law_kim_mccalla_breuhaus_et al._2013, title={Polyomavirus-Associated Nephritis in 2 Horses}, volume={50}, ISSN={0300-9858 1544-2217}, url={http://dx.doi.org/10.1177/0300985813476063}, DOI={10.1177/0300985813476063}, abstractNote={Polyomaviruses produce latent and asymptomatic infections in many species, but productive and lytic infections are rare. In immunocompromised humans, polyomaviruses can cause tubulointerstitial nephritis, demyelination, or meningoencephalitis in the central nervous system and interstitial pneumonia. This report describes 2 Standardbred horses with tubular necrosis and tubulointerstitial nephritis associated with productive equine polyomavirus infection that resembles BK polyomavirus nephropathy in immunocompromised humans.}, number={5}, journal={Veterinary Pathology}, publisher={SAGE Publications}, author={Jennings, S. H. and Wise, A. G. and Nickeleit, V. and Maes, R. K. and Cianciolo, R. E. and Piero, F. Del and Law, J. M. and Kim, Y. and McCalla, A. C. and Breuhaus, B. A. and et al.}, year={2013}, month={Feb}, pages={769–774} }
 @article{breuhaus_2011, title={Disorders of the Equine Thyroid Gland}, volume={27}, ISSN={["1558-4224"]}, DOI={10.1016/j.cveq.2010.12.002}, abstractNote={Regulatory control of the thyroid gland in horses is similar to other species. Clinical signs of hypothyroidism in adult horses are minimal. Several drugs and physiologic and pathophysiological states can cause circulating thyroid hormone concentrations to be low without actual pathology of the thyroid gland. Thus, nonthyroidal factors must be ruled out before a diagnosis of hypothyroidism can be made. Thyroid hormone supplementation seems to be well tolerated, even in euthyroid horses. Neonatal foals have very high circulating thyroid hormone concentrations, and deficiencies result in significant clinical signs. Unlike in adults, two syndromes of hypothyroidism are well described in foals.}, number={1}, journal={VETERINARY CLINICS OF NORTH AMERICA-EQUINE PRACTICE}, author={Breuhaus, Babetta A.}, year={2011}, month={Apr}, pages={115-+} }
 @inbook{breuhaus_2011, title={Endocrine system}, ISBN={9781840761191 9781840766080}, url={http://dx.doi.org/10.1201/b15185-7}, DOI={10.1201/b15185-7}, booktitle={Equine Clinical Medicine, Surgery and Reproduction}, publisher={CRC Press}, author={Breuhaus, Babetta}, year={2011}, month={Mar}, pages={619–636} }
 @article{merlo_sheats_elce_hunter_breuhaus_2009, title={Outbreak of Lawsonia intracellularis on a Standardbred breeding farm in North Carolina}, volume={21}, ISSN={["2042-3292"]}, DOI={10.2746/095777309X400333}, abstractNote={Summary Lawsonia intracellularis is a cause of protein‐losing enteropathy in weanling foals commonly causing signs including diarrhoea, oedema and unthrifty appearance. It has previously been reported as sporadic cases throughout the USA, Canada and Europe. Only recently have outbreaks on a single farm location been reported. The cases reported here are an example of multiple foals on a single farm testing serologically positive for L. intracellularis. These foals ranged in severity from asymptomatic to severely hypoproteinaemic and septic; however, none of the foals ever displayed diarrhoea, which is the most common presenting sign of this disease process.}, number={4}, journal={EQUINE VETERINARY EDUCATION}, author={Merlo, J. L. and Sheats, M. K. and Elce, Y. and Hunter, S. and Breuhaus, B. A.}, year={2009}, month={Apr}, pages={179–182} }
 @article{breuhaus_2009, title={Thyroid Function in Anhidrotic Horses}, volume={23}, ISSN={["1939-1676"]}, DOI={10.1111/j.1939-1676.2008.0217.x}, abstractNote={This study was performed to determine whether anhidrotic horses have altered thyroid function compared with horses that sweat normally.Anhidrotic horses have normal thyroid function.Ten client-owned horses with clinical signs of anhidrosis were paired with 10 horses living in the same environment that had normal sweat production.Horses were diagnosed as having normal sweat production or being anhidrotic based on responses to intradermal injections of terbutaline and physiologic responses to lunging exercise. Control horses were selected from the same environment and matched as closely as possible to anhidrotic horses in terms of age, sex, breed, and athletic condition. Thyrotropin-releasing hormone (TRH) stimulation tests were performed in both horses at the same time, once in the summer or fall, and once again in winter.Anhidrotic horses produced less sweat in response to intradermal injections of terbutaline and exercise than did control horses. They also had greater increases in body temperature and respiratory rate in response to exercise. Resting concentrations of thyroid hormones and thyroid-stimulating hormone (TSH) were not different between anhidrotic and control horses. Thyroid hormone responses to TRH also were not different between the 2 groups of horses. However, anhidrotic horses had a significantly different TSH response to TRH compared with control horses, particularly in the winter.The biologic relevance of the altered TSH response to TRH in anhidrotic horses is uncertain, considering that TSH concentrations remained within previously reported normal ranges and thyroid hormone responses were not different between anhidrotic and control horses.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Breuhaus, B. A.}, year={2009}, pages={168–173} }
 @inbook{breuhaus_2009, place={St. Louis, MO}, edition={6th edition.}, title={Thyroid disease}, booktitle={Current therapy in equine medicine}, publisher={Saunders Elsevier}, author={Breuhaus, B.A.}, editor={Robinson, Ne and Sprayberry, KaEditors}, year={2009}, pages={737–740} }
 @article{johansson_gardner_atkins_lafevers_breuhaus_2007, title={Cardiovascular effects of acute pulmonary obstruction in horses with recurrent airway obstruction}, volume={21}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2007)21[302:CEOAPO]2.0.CO;2}, abstractNote={Recurrent airway obstruction (RAO) is common in horses. Although pulmonary artery (PA) pressure increases during RAO, cardiac function in horses with RAO has received limited attention.The purpose of this study was to noninvasively determine the cardiovascular effects of acute pulmonary obstruction (APO) in horses with RAO and their reversibility.Five geldings with RAO, inducible by exposure to moldy hay, were studied.Pulmonary mechanics, echocardiography, serum troponin I concentrations, arterial blood gases, and hematocrit were obtained before and after 7 days of APO. Heart rate, PA diameter and flow characteristics, right and left ventricular luminal dimensions and wall thicknesses, global cardiac performance, and evidence of myocardial damage were evaluated. Pulmonary mechanics and echocardiography were reevaluated during remission.[corrected] Severe, transient APO did not induce chronic cor pulmonale in horses, because cardiac anatomy and function were normal between episodes. An acute episode of APO produced anatomical and functional cardiac changes in both the right and left heart (including increased PA diameter, abnormal septal motion, and decreased left ventricular diameter and estimated stroke volume), possibly because of the development of pulmonary hypertension, without apparent myocardial damage. The decrease in stroke volume was offset by the increase in heart rate.With APO of 7 days' duration, cardiovascular abnormalities and the functional airway changes that produce them are reversible when the offending allergens are removed.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, Anna M. and Gardner, Sarah Y. and Atkins, Clarke E. and LaFevers, D. Heath and Breuhaus, Babetta A.}, year={2007}, pages={302–307} }
 @article{fogle_gerard_johansson_breuhaus_blikslager_jones_2007, title={Spontaneous rupture of the guttural pouch as a complication of treatment for guttural pouch empyema}, volume={19}, ISSN={["0957-7734"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-34547981740&partnerID=MN8TOARS}, DOI={10.2746/095777307X196900}, abstractNote={Equine Veterinary EducationVolume 19, Issue 7 p. 351-355 Spontaneous rupture of the guttural pouch as a complication of treatment for guttural pouch empyema C. A. Fogle, Corresponding Author C. A. Fogle Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.*Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorM. P. Gerard, M. P. Gerard Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. M. Johansson, A. M. Johansson Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorB. A. Breuhaus, B. A. Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. T. Blikslager, A. T. Blikslager Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author C. A. Fogle, Corresponding Author C. A. Fogle Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.*Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorM. P. Gerard, M. P. Gerard Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. M. Johansson, A. M. Johansson Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorB. A. Breuhaus, B. A. Breuhaus Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorA. T. Blikslager, A. T. Blikslager Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA.Search for more papers by this author First published: 05 January 2010 https://doi.org/10.2746/095777307X196900Citations: 14AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References Adkins, A.R., Yovich, J.V. and Colbourne, C.M. (1997) Nonsurgical treatment of chondroids of the guttural pouch in a horse. Aust. vet. J. 75, 332–333. 10.1111/j.1751-0813.1997.tb15703.x CASPubMedWeb of Science®Google Scholar Bentz, B.G., Dowd, A.L. and Freeman, D.E. (1996) Treatment of guttural pouch empyema with acetylcysteine irrigation. Equine Pract. 18, 33–35. Web of Science®Google Scholar Freeman, D.E. (1991) Guttural pouches. In: Equine Respiratory Disorders, Ed: J. Beech, Lea and Febiger, Philadelphia. pp 305–328. Web of Science®Google Scholar Freeman, D.E. (1999) Guttural pouch. In: Equine Surgery, Eds: J.A. Auer and J.A. Stick, W.B. Saunders, Philadelphia. pp 368–375. Google Scholar Hawkins, J.F., Frank, N., Sojka, J.E. and Levy, M. (2001) Fistulation of the auditory tube diverticulum (guttural pouch) with a neodymiumyttrium-aluminum-garnet laser for treatment of chronic empyema in two horses. J. Am. vet. med. Ass. 218, 405–407. 10.2460/javma.2001.218.405 CASPubMedWeb of Science®Google Scholar Judy, C.E., Chaffin, M.K. and Cohen, N.D. (1999) Empyema of the guttural pouch (auditory tube diverticulum) in horses: 91 cases (1977–1997). J. Am. vet. med. Ass. 215, 1666–1670. CASPubMedWeb of Science®Google Scholar McAllister, E.S. (1978) Guttural pouch disease. Proc. Am. Ass. equine Practnrs. 23, 251–256. Web of Science®Google Scholar Perkins, G.A., Pease, A., Crotty, E. and Fubini, S.L. (2003) Diagnosing guttural pouch disorders and managing guttural pouch empyema in adult horses. Comp. cont. Educ. pract. Vet. 25, 966–973. Web of Science®Google Scholar Citing Literature Volume19, Issue7August 2007Pages 351-355 ReferencesRelatedInformation}, number={7}, journal={EQUINE VETERINARY EDUCATION}, author={Fogle, C. A. and Gerard, M. P. and Johansson, A. M. and Breuhaus, B. A. and Blikslager, A. T. and Jones, S. L.}, year={2007}, month={Aug}, pages={351–355} }
 @article{merlo_breuhaus_schramme_2007, title={What is your diagnosis?}, volume={230}, ISSN={["0003-1488"]}, DOI={10.2460/javma.230.2.193}, number={2}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Merlo, Jennifer L. and Breuhaus, Betta and Schramme, Michael}, year={2007}, month={Jan}, pages={193–194} }
 @article{breuhaus_2006, title={Endocrine diseases of older horses}, journal={Ahead of the curve: OVMA Conference Proceedings, 26-28 January, 2006}, publisher={Milton, Ont. : Ontario Veterinary Medical Association}, author={Breuhaus, B. A.}, year={2006} }
 @article{breuhaus_refsal_beyerlein_2006, title={Measurement of free thyroxine concentration in horses by equilibrium dialysis}, volume={20}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2006)20[371:MOFTCI]2.0.CO;2}, abstractNote={The purpose of the study reported here was to validate measurement of free thyroxine (fT4) concentration in equine serum by equilibrium dialysis (fT4D), and to compare values with fT4 concentration measured directly and with total T4 (TT4) concentration. The fT4D, fT74, and TT4 concentrations were measured over a range of values in euthyroid horses and horses made hypothyroid by administration of propylthiouracil (PTU). Concentrations of fT4D (<1.8–83 pmol/L) were consistently higher than those of fT4 (<1–40 pmol/L). There was a significant (P < .001) regression of fT4D on fT4 in 503 samples from normal horses (y = 2.086x - 0.430). In baseline samples from 71 healthy euthyroid horses, fT4 concentration ranged from 6- 21 pmol/L (median, 11 pmol/L; 95% confidence interval [CI]10.5–11.8 pmol/L), and fT4D concentration ranged from 7–47 pmol/L (median, 22 pmol/L; 95% CI 20.9–25.1 pmol/L). Free T4D, fT4, and TT4 concentrations were also measured in 34 ill horses. Horses consuming PTU and ill horses had significantly (P < .05) lower serum concentration of TT4, fT4, and fT4D than did clinically normal, healthy horses. If serum samples from ill horses were further subdivided into samples from horses that lived and samples from horses that died, fT4D concentration was not significantly different in ill horses that lived, compared with that in healthy horses, whereas fT4 concentration was still significantly decreased in ill horses that died (P < 0.001). We conclude that measurement of fT4 concentration by equilibrium dialysis is a valid technique in the horse, and its use may provide improved ability to distinguish nonthyroidal illness syndrome from hypothyroidism in that species.}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Breuhaus, BA and Refsal, KR and Beyerlein, SL}, year={2006}, pages={371–376} }
 @inproceedings{breuhaus_2006, title={Thyroid function and dysfunction in equine neonates}, booktitle={Proceedings of the 2006 American College of Veterinary Internal Medicine Conference}, author={Breuhaus, B.A.}, year={2006}, pages={162–164} }
 @article{rothschild_hines_breuhaus_gay_sellon_2004, title={Effects of trimethoprim-sulfadiazine on thyroid function of horses}, volume={18}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2004)18<370:EOTOTF>2.0.CO;2}, abstractNote={Trimethoprim-sulfadiazine was administered to horses in a randomized, placebo controlled study to determine the effects of potentiated sulfonamides on thyroid function in normal horses. The treatment group included eight horses that received trimethoprim-sulfadiazine mixed with molasses orally at 30 mg/kg once daily for eight weeks. The control group included 8 horses that received an oral placebo (flour mixed with molasses) once daily for the same period. Thyroid function was evaluated prior to initiation of treatment and after 8 weeks of treatment. Serum concentrations of total and free triiodothyronine (T3), total and free thyroxine (T4), and thyroid stimulating hormone (TSH) were determined at rest and after a thyrotropin-releasing hormone (TRH) stimulation test. There was no detectable difference between treatment and control groups.}, number={3}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Rothschild, CM and Hines, MT and Breuhaus, B and Gay, J and Sellon, DC}, year={2004}, pages={370–373} }
 @inproceedings{breuhaus_2004, title={Review of thyroid function and dysfunction in adult horses}, volume={50}, booktitle={Proceedings of the 50th Annual Convention of the American Association of Equine Practitioners}, author={Breuhaus, B.A.}, year={2004}, pages={334–337} }
 @inproceedings{breuhaus_2003, title={Thyroid function in horses - Uncovering the Myths}, booktitle={Proceedings of the 2003 American College of Veterinary Internal Medicine Conference}, author={Breuhaus, B.A.}, year={2003} }
 @article{breuhaus_2003, title={Thyroid function in mature horses ingesting endophyte-infected fescue seed}, volume={223}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2003.223.340}, abstractNote={Abstract Objective —To determine whether ingestion of fescue seed infected with the endophyte Neotyphodium coenophialum would alter thyroid function in adult horses. Design —Original study. Animals —4 adult mares that were not pregnant and 6 adult geldings. Procedure —Thyrotropin releasing hormone stimulation tests were performed while horses received a standard diet and after infected seed (2.3 kg/d [5 lb/d]) had been fed for 1 and 2 months. Serum prolactin concentrations were measured to verify endophyte absorption. Results —Serum prolactin concentrations indicated that at least 8 of 10 horses absorbed the endophyte. Baseline concentrations of thyroid stimulating hormone, total and free triiodothyronine, and total and free thyroxine and the change in hormone concentrations in response to administration of thyrotropin releasing hormone (1 mg, IV) were not altered by ingestion of endophyte-infected fescue seed. Conclusions and Clinical Relevance —Results suggest that ingestion of fescue seed infected with the endophytic fungus N coenophialum for 2 months has little effect on thyroid function in adult horses that are not pregnant. ( J Am Vet Med Assoc 2003;223:340–345)}, number={3}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Breuhaus, BA}, year={2003}, month={Aug}, pages={340–345} }
 @article{davis_gardner_schwabenton_breuhaus_2002, title={Congestive heart failure in horses: 14 cases (1984-2001)}, volume={220}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2002.220.1512}, abstractNote={To identify clinical signs, underlying cardiac conditions, echocardiographic findings, and prognosis for horses with congestive heart failure.Retrospective study.14 horses.Signalment; history; clinical signs; clinicopathologic, echocardiographic, and radiographic findings; treatment; and outcome were determined by reviewing medical records.All 14 horses were examined because of a heart murmur; tachycardia was identified in all 14. Twelve horses had echocardiographic evidence of enlargement of 1 or more chambers of the heart. Other common clinical findings included jugular distention or pulsation, crackles, cough, tachypnea, and ventral edema. Nine horses had signs consistent with heart failure for > 6 days. Underlying causes for heart failure included congenital defects, traumatic vascular rupture, pericarditis, pulmonary hypertension secondary to heaves, and valvular dysplasia. Seven horses were euthanatized after diagnosis of heart failure; 5 were discharged but were euthanatized or died of complications of heart disease within 1 year after discharge. The remaining 2 horses were discharged but lost to follow-up.Results suggest that congestive heart failure is rare in horses. A loud heart murmur accompanied by either jugular distention or pulsation, tachycardia, respiratory abnormalities (crackles, cough, tachypnea), and ventral edema were the most common clinical signs. Echocardiography was useful in determining the underlying cause in affected horses. The long-term prognosis for horses with congestive heart failure was grave.}, number={10}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Davis, JL and Gardner, SY and Schwabenton, B and Breuhaus, BA}, year={2002}, month={May}, pages={1512–1515} }
 @article{breuhaus_2002, title={Thyroid-stimulating hormone in adult euthyroid and hypothyroid horses}, volume={16}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2002)016<0109:TSHIAE>2.3.CO;2}, abstractNote={The purpose of this study was to validate a thyroid-stimulating hormone (TSH) assay in a model of equine hypothyroidism. Thyrotropin-releasing hormone (TRH) stimulation tests were performed in 12 healthy adult mares and geldings, aged 4 to greater than 20 years, before and during administration of the antithyroid drug propylthiouracil (PTU) for 6 weeks. Serum concentrations of equine TSH, total and free thyroxine (T4), and total and free triiodothyronine (T3) were measured. Before PTU administration, mean ± standard deviation baseline concentrations of TSH were 0.40 ± 0.29 ng/mL. TSH increased in response to TRH, reaching a peak concentration of 0.78 ± 0.28 ng/mL at 45 minutes. Total and free T4 increased from 12.9 ± 5.6 nmol/L and 12.2 ± 3.5 pmol/L to 36.8 ± 11.4 nmol/L and 23.1 ± 5.9 pmol/L, respectively, peaking at 4–6 hours. Total and free T3 increased from 0.99 ± 0.51 nmol/L and 2.07 ± 1.14 pmol/L to 2.23 ± 0.60 nmol/L and 5.78 ± 1.94 pmol/L, respectively, peaking at 2–4 hours. Weekly measurements of baseline TSH and thyroid hormones during PTU administration showed that total and free T3 concentrations fell abruptly and remained low throughout PTU administration. Total and free T4 concentrations did not decrease dramatically until weeks 5 and 4 of PTU administration, respectively. A steady increase in TSH concentration occurred throughout PTU administration, with TSH becoming markedly increased by weeks 5 and 6 (1.46 ± 0.94 ng/mL at 6 weeks). During weeks 5 and 6 of PTU administration, TSH response to TRH was exaggerated, and thyroid hormone response was blunted. Results of this study show that measurement of equine TSH in conjunction with thyroid hormone measurement differentiated normal and hypothyroid horses in this model of equine hypothyroidism.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Breuhaus, BA}, year={2002}, pages={109–115} }
 @article{guy_breslin_breuhaus_vivrette_smith_2000, title={Characterization of a coronavirus isolated from a diarrheic foal}, volume={38}, number={12}, journal={Journal of Clinical Microbiology}, author={Guy, J. S. and Breslin, J. J. and Breuhaus, B. and Vivrette, S. and Smith, L. G.}, year={2000}, pages={4523–4526} }
 @article{sellon_spaulding_breuhaus_katz_mealey_2000, title={Hepatic abscesses in three horses}, volume={216}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2000.216.882}, abstractNote={Hepatic abscesses were diagnosed in 3 adult horses. Two were < 4 years old and had evidence of concurrent immune-mediated conditions, including aseptic arthritis, immune-mediated thrombocytopenia, and immune-mediated anemia. Predisposing factors for hepatic abscess formation in these horses included prior abdominal surgery, proximal duodenitis/jejunitis, inflammatory bowel disease, and a penetrating foreign body in the large colon. Serum hepatic enzyme activities were within or slightly greater then reference limits in all 3 horses. The most pronounced and consistent abnormalities on CBC and serum biochemical analyses were hyperproteinemia, hyperglobulinemia, and a decreased albumin-to-globulin concentration ratio. Hepatic ultrasonography identified hepatic abscesses in all 3 horses. A variety of bacteria were isolated from these abscesses, including Staphylococus aureus and Bacteroides fragilis. One horse developed septic tibiotarsal arthritis, presumably as a result of intermittent bacteremia. Despite aggressive medical treatment, all horses were euthanatized because of a worsening condition and poor prognosis.}, number={6}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Sellon, DC and Spaulding, K and Breuhaus, BA and Katz, L and Mealey, R}, year={2000}, month={Mar}, pages={882-+} }
 @article{breuhaus_degraves_honore_papich_1999, title={Pharmacokinetics of ibuprofen after intravenous and oral administration and assessment of safety of administration to healthy foals}, volume={60}, number={9}, journal={American Journal of Veterinary Research}, author={Breuhaus, B. A. and Degraves, F. J. and Honore, E. K. and Papich, M. G.}, year={1999}, pages={1066–1073} }
 @article{jorgensen_geoly_berry_breuhaus_1997, title={Lameness and pleural effusion associated with an aggressive fibrosarcoma in a horse}, volume={210}, number={9}, journal={Journal of the American Veterinary Medical Association}, author={Jorgensen, J. S. and Geoly, F. J. and Berry, C. R. and Breuhaus, B. A.}, year={1997}, pages={1328–1331} }
 @article{mcginnes_mansmann_breuhaus_1996, title={Nasogastric electrolyte replacement in horses}, volume={18}, number={8}, journal={Compendium on Continuing Education for the Practicing Veterinarian}, author={McGinnes, S.G. and Mansmann, R.A. and Breuhaus, B.A.}, year={1996}, pages={942–951} }
 @article{breuhaus_degraves_1993, title={PLASMA ENDOTOXIN CONCENTRATIONS IN CLINICALLY NORMAL AND POTENTIALLY SEPTIC EQUINE NEONATES}, volume={7}, ISSN={["0891-6640"]}, DOI={10.1111/j.1939-1676.1993.tb01022.x}, abstractNote={Plasma endotoxin concentrations were measured at 1 to 2 and 5 to 6 days of age in clinically normal foals and in potentially septic neonatal foals admitted to North Carolina State University's Veterinary Teaching Hospital for a variety of conditions. In 1 to 2 and 5 to 6 day old normal foals, median plasma endotoxin concentrations were 2.17 (range, 1.61-2.54; n = 6) and 2.89 (range, 2.61-3.50; n = 7) endotoxin units/mL (EU/mL), respectively. Median plasma endotoxin concentration in potentially septic foals with negative blood cultures or gram positive isolates (n = 8) was 2.73 (range, 0.59-4.04) EU/mL. In hospitalized foals with gram negative isolates (n = 6), median plasma endotoxin concentration was 78.06 (range, 0.76-2,696.41) EU/mL, but individual endotoxin values were only increased in foals that were extremely sick and died within hours of sampling. Plasma endotoxin concentrations were significantly greater in foals with sepsis scores > or = 11 compared with foals with sepsis scores < or = 10. Increased plasma endotoxin concentrations appear to predict an unfavorable outcome in septic foals, but normal endotoxin concentrations do not appear to have any predictive value.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={BREUHAUS, BA and DEGRAVES, FJ}, year={1993}, pages={296–302} }
 @article{wichtel_breuhaus_aucoin_1992, title={Relation between pharmacokinetics of amikacin sulfate and sepsis score in clinically normal and hospitalized neonatal foals}, volume={200}, number={9}, journal={Journal of the American Veterinary Medical Association}, author={Wichtel, M.G. and Breuhaus, B.A. and Aucoin, D.}, year={1992}, month={Apr}, pages={1339–1343} }
 @article{specht_breuhaus_manning_miller_cochrane_1991, title={Skin pustules and nodules caused by Actinomyces viscosus in a horse}, volume={198}, number={3}, journal={Journal of the American  Veterinary Medical Association}, author={Specht, T.E. and Breuhaus, B.A. and Manning, T.O. and Miller, R.T. and Cochrane, R.B.}, year={1991}, month={Jan}, pages={457–459} }
 @article{breuhaus_chimoskey_1990, title={HEMODYNAMIC AND BEHAVIORAL-EFFECTS OF ANGIOTENSIN-II IN CONSCIOUS SHEEP}, volume={258}, ISSN={["0002-9513"]}, DOI={10.1152/ajpregu.1990.258.5.r1230}, abstractNote={Intracerebroventricular (ivt) angiotensin II (ANG II) at 0.4, 2, 10, and 50 ng.kg-1.min-1 increased arterial pressure in conscious sheep in a dose-related manner (26 mmHg, P less than 0.05, at 50 ng.kg-1.min-1). Total peripheral resistance (TPR) and right atrial pressure also increased. Heart rate, stroke volume, and cardiac output did not change. Pressor responses to ivt ANG II were not caused by leakage of ANG II into the periphery, because plasma concentrations of ANG II did not change from control (31 +/- 7 pg/ml) at the highest dose of ANG II infused. In contrast, intravenous (iv) ANG II, 10 and 50 ng.kg-1.min-1, increased arterial pressure 29 and 47 mmHg, respectively (P less than 0.05), and decreased heart rate. ANG II, 10 ng.kg-1.min-1 iv, increased plasma ANG II levels from 36 +/- 6 to 354 +/- 69 pg/ml (P less than 0.05). Intracarotid (ic) ANG II, 10 ng.kg-1.min-1, increased arterial pressure 31 mmHg (P less than 0.05) but did not alter heart rate. ANG II ivt caused a dose-related drinking response, with a positive correlation between the amount of water drunk during ivt ANG II infusion and the increase in arterial pressure. Infusions of ANG II at 50 ng.kg-1.min-1 ivt were associated with decreased plasma osmolality and potassium concentration and increased plasma vasopressin concentration.}, number={5}, journal={AMERICAN JOURNAL OF PHYSIOLOGY}, author={BREUHAUS, BA and CHIMOSKEY, JE}, year={1990}, month={May}, pages={R1230–R1237} }
 @inproceedings{bowman_riviere_aucoin_breuhaus_1990, title={Septic arthritis: use of therapeutic monitoring to optimize antibiotic therapy}, volume={36}, booktitle={Proceedings of the Annual Convention of the American Association of Equine Practitioners}, author={Bowman, K. F. and Riviere, J. E. and Aucoin, D. P. and Breuhaus, B. A.}, year={1990}, pages={125–131} }
 @article{breuhaus_demarest_chimoskey_1989, title={Comparison of intracerebroventricular and intracarotid infusions of PGE2 in conscious sheep}, volume={256}, ISSN={0363-6119 1522-1490}, url={http://dx.doi.org/10.1152/ajpregu.1989.256.3.r685}, DOI={10.1152/ajpregu.1989.256.3.r685}, abstractNote={Conscious sheep chronically prepared with nonocclusive indwelling vascular and cerebroventricular catheters were used to compare hemodynamic, hematologic, hormonal, and behavioral responses of intracarotid (ic) prostaglandin E2 (PGE2) to intracerebroventricular (ivt) PGE2. PGE2 had less potent hemodynamic effects when infused ivt than when infused ic. Intracarotid PGE2, 100 ng.kg-1.min-1, increased arterial pressure and heart rate 31 mmHg and 26 beats/min, respectively (P less than 0.01), whereas ivt PGE2, 300 ng.kg-1.min-1, did not alter heart rate and increased arterial pressure 9 mmHg (P less than 0.01). Both ic and ivt PGE2 increased packed cell volume 3% (P less than 0.01). Neither ic nor ivt PGE2 caused changes in plasma concentrations of epinephrine or norepinephrine. Despite ivt PGE2S less potent hemodynamic effects, ivt administration of PGE2 decreased plasma osmolality 2 mosmol/kg (P less than 0.05) and sodium concentration 2 meq/l (P less than 0.01) and increased plasma vasopressin concentration 2.5-fold (P less than 0.05). Intracerebroventricular PGE2 also caused some physical and behavioral changes that were not observed during ic PGE2 administration or during ivt infusion of vehicle. These changes included pupillary constriction, vocalization, and coughing. We conclude that PGE2 given ivt may not reach the same sites in the brain as does ic PGE2 or that ivt PGE2 may reach the same sites in different concentrations.}, number={3}, journal={American Journal of Physiology-Regulatory, Integrative and Comparative Physiology}, publisher={American Physiological Society}, author={Breuhaus, B. A. and Demarest, K. T. and Chimoskey, J. E.}, year={1989}, month={Mar}, pages={R685–R693} }
 @article{breuhaus_chimoskey_1987, title={Central angiotensin II and PGE2 act independently to increase blood pressure in conscious sheep}, volume={252}, ISSN={0363-6119 1522-1490}, url={http://dx.doi.org/10.1152/ajpregu.1987.252.1.r73}, DOI={10.1152/ajpregu.1987.252.1.r73}, abstractNote={Conscious adult female sheep chronically prepared with nonocclusive indwelling vascular and cerebroventricular catheters were used to determine whether centrally administered prostaglandin E2 (PGE2) increases blood pressure by activation of the brain renin angiotensin system or whether centrally administered angiotensin II (ANG II) increases blood pressure by stimulating prostaglandin synthesis in the brain. Intracerebroventricular (ivt) ANG II, 50 ng X kg-1 X min-1, increased arterial pressure 23 mmHg (P less than 0.01) 30 min after the start of infusion. Infusion of the ANG II antagonist [Sar1-Thr8]ANG II (sarthran), 1,000 ng X kg-1 X min-1 ivt, had no effect on arterial pressure when given by itself but reduced the ivt ANG II-induced pressor response to 5 mmHg (P less than 0.05) when the two peptides were infused at the same time. Intracerebroventricular infusion of sarthran did not alter the pressor responses to intracarotid (ic) PGE2 or to ivt PGE2. Blood pressure increased 21 mmHg (P less than 0.01) 30 min after the start of PGE2 infusion when PGE2 was given ic by itself, compared with 17 mmHg (P less than 0.01) when PGE2 was given ic at the same time as sarthran was given ivt. Blood pressure increased 14 mmHg (P less than 0.01) 30 min after the start of PGE2 infusion when PGE2 was given ivt by itself, compared with 16 mmHg (P less than 0.01) when PGE2 was given ivt at the same time as sarthran was given ivt. Pretreatment with the cyclooxygenase inhibitors indomethacin, 4 mg/kg sc, or flunixin meglumine, 3 mg/kg iv, did not alter the ivt ANG II-induced pressor response.(ABSTRACT TRUNCATED AT 250 WORDS)}, number={1}, journal={American Journal of Physiology-Regulatory, Integrative and Comparative Physiology}, publisher={American Physiological Society}, author={Breuhaus, B. A. and Chimoskey, J. E.}, year={1987}, month={Jan}, pages={R73–R77} }
 @inproceedings{breuhaus_chimoskey_saneii_sparks_wangler_1986, title={Synthetic (23 amino acid) atrial natriuretic peptide lowers cardiac output in conscious sheep and constricts coronary arteries in isolated guinea pig hearts}, volume={371}, booktitle={Journal of Physiology}, author={Breuhaus, B.A. and Chimoskey, J.E. and Saneii, H.H. and Sparks, H.V. and Wangler, R.D.}, year={1986}, month={Dec}, pages={82} }
 @article{breuhaus_saneii_brandt_chimoskey_1985, title={Atriopeptin II lowers cardiac output in conscious sheep}, volume={249}, ISSN={0363-6119 1522-1490}, url={http://dx.doi.org/10.1152/ajpregu.1985.249.6.r776}, DOI={10.1152/ajpregu.1985.249.6.r776}, abstractNote={Atrial natriuretic peptides cause natriuresis, kaliuresis, diuresis, and hypotension. They relax vascular smooth muscle in vitro, and they dilate renal vessels in vivo. Hence, we tested the hypothesis that they produce hypotension by lowering total peripheral resistance. The studies were performed in conscious chronically instrumented sheep standing quietly in their cages. Atriopeptin II (AP II) was infused into the right atrium for 30 min at 0.1 nmol X kg-1 X min-1. Atriopeptin II lowers arterial pressure (9%, P less than 0.05) by lowering cardiac output (18%, P less than 0.05), stroke volume (28%, P less than 0.05), and right atrial pressure (2.3 mmHg, P less than 0.05). Heart rate and total peripheral resistance increase (16 and 13%, respectively, P less than 0.05). Partial ganglionic blockade with trimethaphan camsylate during AP II infusion prevents the increases in heart rate and total peripheral resistance. The changes in right atrial pressure, stroke volume, and cardiac output persist, and arterial pressure falls further (27%, P less than 0.05). These hemodynamic data are consistent with direct AP II-induced relaxation of venous smooth muscle with reduction of venous return, right atrial pressure, stroke volume, cardiac output, and arterial pressure, followed by reflex activation of the sympathetic nervous system to increase heart rate and total peripheral resistance. Because partial ganglionic blockade alone and AP II alone cause similar reductions in right atrial pressure (2.1 and 2.3 mmHg, respectively) but AP II causes a greater fall in stroke volume (28 vs. 13%), it is possible that AP II also causes coronary vasoconstriction.}, number={6}, journal={American Journal of Physiology-Regulatory, Integrative and Comparative Physiology}, publisher={American Physiological Society}, author={Breuhaus, B. A. and Saneii, H. H. and Brandt, M. A. and Chimoskey, J. E.}, year={1985}, month={Dec}, pages={R776–R780} }
 @article{wangler_breuhaus_otero_hastings_holzman_saneii_sparks_chimoskey_1985, title={Coronary vasoconstrictor effects of atriopeptin II}, volume={230}, ISSN={0036-8075 1095-9203}, url={http://dx.doi.org/10.1126/science.2931801}, DOI={10.1126/science.2931801}, abstractNote={Atrial natriuretic peptides lower arterial pressure, cardiac filling pressure, and cardiac output. In isolated, Langendorff-perfused guinea pig hearts, atriopeptin II, the 23-amino acid atrial natriuretic peptide, is also a potent coronary vasoconstrictor. The median effective dose for atriopeptin II in guinea pig hearts is 26 nanomoles, the threshold constrictor dose is 5 nanomoles, and flow nearly ceases at a dose of 100 nanomoles in perfused hearts at constant pressure. Similar concentrations of atriopeptin II also cause coronary vasoconstriction in rat and dog heart preparations. The disulfide bridge is necessary for vasoconstrictor activity; reduction of this bridge abolishes the activity, as it does the other biological activities of atrial natriuretic peptides.}, number={4725}, journal={Science}, publisher={American Association for the Advancement of Science (AAAS)}, author={Wangler, R. and Breuhaus, B. and Otero, H. and Hastings, D. and Holzman, M. and Saneii, H. and Sparks, H. and Chimoskey, J.}, year={1985}, month={Nov}, pages={558–561} }
 @article{breuhaus_chimoskey_1985, title={Mechanism of Tachycardia Caused by Intracarotid PGE2 in Conscious Ewes}, volume={180}, ISSN={1535-3702 1535-3699}, url={http://dx.doi.org/10.3181/00379727-180-42188}, DOI={10.3181/00379727-180-42188}, abstractNote={Conscious adult ewes prepared with nonocclusive indwelling vascular catheters were used to determine the mechanism by which heart rate increases during central administration of prostaglandin E2 (PGE2). Heart rate increased 14 bpm during steady-state intracarotid infusion of PGE2, 10 ng/kg/min (P less than 0.05). Intravenous atropine methyl bromide, 1 mg/kg, increased heart rate 26 bpm (P less than 0.05) 5 min after injection. Heart rate remained elevated 30 min after injection. The heart rate response to PGE2 plus atropine was greater than the heart rate response to either atropine or PGE2 alone (P less than 0.05). Propranolol, 1 mg/kg bolus plus intravenous infusion, 0.025 mg/kg/min, did not change resting heart rate. Propranolol attenuated but did not abolish the increase in heart rate caused by intracarotid PGE2. Although heart rate increased in response to PGE2 after administration of either propranolol or atropine alone, the combination of propranolol and atropine prevented any further increase in heart rate during subsequent PGE2 infusion. The increase in heart rate when all three drugs were given together was not different from the increase observed during atropine alone. Thus, both beta-adrenergic activation and muscarinic deactivation contribute to the PGE2-induced tachycardia.}, number={2}, journal={Experimental Biology and Medicine}, publisher={SAGE Publications}, author={Breuhaus, B. A. and Chimoskey, J. E.}, year={1985}, month={Nov}, pages={353–358} }
 @article{chimoskey_breuhaus_ely_1983, title={Cardiac and Sinoaortic Reflexes During Aortic Constriction in Awake Calves}, volume={11}, ISSN={0090-5488}, url={http://dx.doi.org/10.3109/10731198309118805}, DOI={10.3109/10731198309118805}, abstractNote={The hemodynamic responses to increased afterload of the left ventricle were studied in conscious calves before and during cooling of the cervical vagus nerves bilaterally. The calves were chronically instrumented to measure (or derive) heart rate, stroke volume, cardiac output, iliac, superior mesenteric and renal flows and resistances, mean aortic, right atrial, pulmonary artery, and left atrial pressures, the systemic and pulmonary pressure gradients, and total systemic and total pulmonary resistances. The calves were also instrumented to produce reversible partial constriction of the ascending aorta and for cooling of the cervical vagus nerves. The hemodynamic responses to increased afterload were characterized before and during bilateral cervical vagus nerve cooling to 6–7°C. Aortic constriction causes stroke volume, cardiac output and aortic pulse pressure to decrease. Left atrial pressure and total peripheral resistance increase. Mean aortic pressure is constant during aortic constriction alone, despite a continued decrease in pulse pressure, due to a balance between sinoaortic reflexes which attempt to increase arterial pressure in response to the decreased pulse pressure and cardiopulmonary reflexes which attempt to decrease arterial pressure in response to the increased left atrial and cardiopulmonary pressures. Vagal cooling removes cardiopulmonary reflex modulation of the sinoaortlc reflexes. During aortic constriction and vagal cooling, the carotid sinus reflex, acting alone, causes large increases in renal and total peripheral resistance and mean aortic pressure.}, number={2-3}, journal={Biomaterials, Medical Devices, and Artificial Organs}, publisher={Informa UK Limited}, author={Chimoskey, John E. and Breuhaus, Babetta A. and Ely, Stephen W.}, year={1983}, month={Jan}, pages={175–195} }
 @article{breuhaus_brown_scott_ainsworth_taylor_1983, title={Clostridial muscle infections following intramuscular injections in the horse}, volume={3}, ISSN={0737-0806}, url={http://dx.doi.org/10.1016/s0737-0806(83)80003-3}, DOI={10.1016/s0737-0806(83)80003-3}, abstractNote={A variety of diseases have been associated with Clostridium species in the horse, including tetanus, botulism, enteritis, enterotoxemia, hepatic abscesses, hepatic necrosis, and myonecrosis, with and without cellulitis.~ 15 In humans, clostridial diseases are generally classified by disease syndrome rather than by causative organism (e.g. gas gangrene, septicemia, gastroenteritis or food poisoning, uterine infections, tetanus, etc.). ~6 Tetanus is caused exclusively by CI. tetani, but the other syndromes can be caused by one or more species, and one species may be capable of causing more than one syndrome. ~6 It is, therefore, accepted in human medicine that the diseases caused by a specific Clostridium may vary depending on local tissue factors, virulence, toxin-producing capability, and potency of toxins produced. Case reports of clostridial muscle infections in the horse describe several different syndromes produced by a variety of clostridial species? 7'8 l~ ~31415 Some of these syndromes have been called malignant edema, others myositis, and one was a focal abscess. In common with other mammalian species? it appears that clostridial infections of equine muscle can produce a variety of clinical syndromes. It is, therefore, p robab ly unwise to a t t em p t a detailed classification based either on the clinical and pathological findings or one based on the causative organisms. In this paper describing 5 horses with clostridial infections of muscles, no attempt to distinguish specific disease entities will be made. It is the authors' opinion that they represent different degrees of the same problem, and reflect the specific local tissue conditions of each infection and the types of toxins produced. Clostridia are large anaerobic Gram-positive sporeforming rods, but can withstand short periods of low oxygen tension. They are commonly found in the soil and in the intestinal tracts of domestic animals. 3 They may also be normal flora of skin and mucous membranes. ~6 Under certain circumstances, infections can develop in muscle. Two modes of infection are believed to exist. 3 The first, typically described as the mechanism of blackleg infection in cattle, suggests that clostridial spores are absorbed from}, number={2}, journal={Journal of Equine Veterinary Science}, publisher={Elsevier BV}, author={Breuhaus, B.A. and Brown, C.M. and Scott, E.A. and Ainsworth, D.M. and Taylor, R.F.}, year={1983}, month={Jan}, pages={42–46} }
 @article{breuhaus_chimoskey_1983, title={PGE2 does not act at carotid sinus to raise arterial pressure in conscious sheep}, volume={245}, ISSN={0363-6135 1522-1539}, url={http://dx.doi.org/10.1152/ajpheart.1983.245.6.h1007}, DOI={10.1152/ajpheart.1983.245.6.h1007}, abstractNote={Conscious chronically instrumented adult female sheep were used to determine whether direct action of prostaglandin E2 (PGE2) on the carotid sinus baroreceptors contributes to the pressor response observed during infusion of PGE2 into the common carotid artery (CCA). During infusion of PGE2 into the CCA caudal to an intact carotid sinus, into the CCA caudal to a denervated carotid sinus, and into the external carotid artery, mean arterial pressure (MAP) rose 17, 22, and 17 mmHg, respectively (P less than 0.01). Heart rate (HR) rose 6, 6, and 8 beats/min, respectively (P less than 0.05). Cardiac output (CO) was also measured by indicator dilution using indocyanine green. In these experiments with infusion of PGE2 into the external carotid artery, MAP rose 15 mmHg (P less than 0.01), HR increased 6 beats/min (P less than 0.05), CO did not change, and total peripheral resistance (TPR) increased 23% (P less than 0.01). With infusion of PGE2 past a denervated carotid sinus, MAP rose 20 mmHg (P less than 0.01), HR rose 4 beats/min (P less than 0.05), CO did not change, and TPR increased 29% (P less than 0.01). There were no statistically significant differences in MAP or HR responses when PGE2 was infused past an intact carotid sinus, past a denervated carotid sinus, or beyond the carotid sinus. There is no evidence that direct action of PGE2 on carotid sinus baroreceptors either augments or inhibits the observed pressor effect of intracarotid PGE2. Intracarotid PGE2 acts rostral to the carotid sinus to increase MAP, HR, and TPR in conscious sheep.}, number={6}, journal={American Journal of Physiology-Heart and Circulatory Physiology}, publisher={American Physiological Society}, author={Breuhaus, B. A. and Chimoskey, J. E.}, year={1983}, month={Dec}, pages={H1007–H1012} }
 @article{chimoskey_breuhaus_ely_1982, title={Hemodynamics of High Afterload Left Heart Failure for Assist Device Testing}, volume={10}, ISSN={0090-5488}, url={http://dx.doi.org/10.3109/10731198209118785}, DOI={10.3109/10731198209118785}, abstractNote={AbstractThe hemodynamic responses to increased afterload of the left ventricle were studied in conscious calves during exercise. The calves were chronically instrumented to measure (or derive) heart rate, stroke volume, cardiac output, iliac, superior mesenteric and renal flows and resistances, mean carotid, aortic, right atrial, pulmonary artery, and left atrial pressures, the systemic and pulmonary pressure gradients, and total systemic and total pulmonary resistances. The calves were also instrumented to produce reversible partial constriction of the ascending aorta and common carotid arteries and for cooling of the cervical vagus nerves. The hemodynamic responses to increased afterload were characterized during treadmill exercise at 2 mph. These responses were compared to the hemodynamic responses to bilateral carotid artery occlusion with and without vagal cooling.}, number={4}, journal={Biomaterials, Medical Devices, and Artificial Organs}, publisher={Informa UK Limited}, author={Chimoskey, John E. and Breuhaus, Babetta A. and Ely, Stephen W.}, year={1982}, month={Jan}, pages={267–279} }
 @article{scott_breuhaus_gertson_1982, title={Surgical repair of dislocated superficial digital flexor tendon in a horse}, volume={181}, number={2}, journal={J Am Vet Med Assoc}, author={Scott, E.A. and Breuhaus, B. and Gertson, K.E.}, year={1982}, pages={171–172} }
 @article{breuhaus_brown_1981, title={Dysphagia associated with soft palate thickening (in the horse)}, volume={3}, number={4}, journal={Equine Practice}, author={Breuhaus, B.A. and Brown, C.M.}, year={1981}, pages={19–23} }