@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}, 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"]}, DOI={10.1111/vde.12982}, abstractNote={BackgroundBullous 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.}, journal={VETERINARY DERMATOLOGY}, 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}, 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={Abstract}, 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. GLIA 2014;62:39–51}, 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}, 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={BackgroundThis study was performed to determine whether sick horses have thyroid hormone (TH) alterations similar to those observed in nonthyroidal illness syndrome in other species.}, 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={BackgroundThis study was performed to compare thyroid function of premature foals to term foals.}, 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}, 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={Background:This study was performed to determine whether anhidrotic horses have altered thyroid function compared with horses that sweat normally.}, 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, fT4, 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}, 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={Abstract}, 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 T, 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 ≥ 11 compared with foals with sepsis scores ≤ 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. (Journal of Veterinary Internal Medicine 1993; 7:296–302. Copyright © 1993 by the American College of Veterinary Internal Medicine.)}, 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={Abstract 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 < 0.05). Intravenous atropine methyl bromide, 1 mg/kg, increased heart rate 26 bpm (P < 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 < 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 β-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 degrees 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 sinoaortic 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={The 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} }