@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{atkins_rausch_gardner_defrancesco_keene_levine_2007, title={The effect of amlodipine and the combination of amlodipine and enalapril on the renin-angiotensin-aldosterone system in the dog}, volume={30}, ISSN={0140-7783 1365-2885}, url={http://dx.doi.org/10.1111/j.1365-2885.2007.00894.x}, DOI={10.1111/j.1365-2885.2007.00894.x}, abstractNote={Excessive aldosterone secretion is detrimental to the heart, vessels and kidneys, contributing to hypertension and the signs and progression of heart failure. Aldosterone secretion, abnormally elevated in heart failure and hypertension, can be blunted with angiotensin‐converting enzyme inhibitors. Amlodipine, used to treat hypertension and heart failure, was hypothesized to activate the renin‐angiotensin‐aldosterone system (RAAS). A study was conducted with six normal adult male beagle dogs. Each dog received amlodipine (0.57 mg/kg b.i.d.) for 6 days, followed by amlodipine (0.57 mg/kg b.i.d.) and enalapril (0.57 mg/kg b.i.d.) for 4 days. Blood pressure, heart rate, serum chemistries and urinary aldosterone excretion, as a measure of RAAS activation, were compared with baseline values. Blood pressure fell by approximately 7% with amlodipine (P = 0.05) and a further 7% with the combination of amlodipine and enalapril (P < 0.01). Blood urea nitrogen increased with the combination (P < 0.05) but only one dog became mildly azotemic. Renin‐angiotensin‐aldosterone system activation, based on 24 h urinary aldosterone excretion and by aldosterone:creatinine ratio was increased by approximately threefold (P < 0.05) with amlodipine administration. This effect was blunted by enalapril, such that aldosterone excretion was no longer different from that observed under control conditions, although values for 24‐h aldosterone excretion did not return to pretreament levels.}, number={5}, journal={Journal of Veterinary Pharmacology and Therapeutics}, publisher={Wiley}, author={Atkins, C. E. and Rausch, W. P. and Gardner, S. Y. and Defrancesco, T. C. and Keene, B. W. and Levine, J. F.}, year={2007}, month={Oct}, pages={394–400} }
 @article{gardner_cook_jortner_troan_sharp_campbell_brownie_2005, title={Stringhalt associated with a pasture infested with Hypochoeris radicata}, volume={17}, DOI={10.1111/j.2042-3292.2005.tb00349.x}, abstractNote={Equine Veterinary EducationVolume 17, Issue 3 p. 118-122 Stringhalt associated with a pasture infested with Hypochoeris radicata S. Y. Gardner, Corresponding Author S. Y. Gardner Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USADepartment of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorA. G. Cook, A. G. Cook Departments of Large Animal Clinical Sciences, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USA Davie County Large Animal Hospital, 928 Farmington Rd, Mocksville, North Carolina 27028, USASearch for more papers by this authorB. S. Jortner, B. S. Jortner Biomedical Sciences and Pathobiology, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USASearch for more papers by this authorB. V. Troan, B. V. Troan Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorN. J. H. Sharp, N. J. H. Sharp Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA Animal Critical Care Group, 1410 Boundary Road, Burnaby, British Columbia V5K 4V3, CanadaSearch for more papers by this authorN. B. Campbell, N. B. Campbell Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorC. F. Brownie, C. F. Brownie Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this author S. Y. Gardner, Corresponding Author S. Y. Gardner Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USADepartment of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorA. G. Cook, A. G. Cook Departments of Large Animal Clinical Sciences, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USA Davie County Large Animal Hospital, 928 Farmington Rd, Mocksville, North Carolina 27028, USASearch for more papers by this authorB. S. Jortner, B. S. Jortner Biomedical Sciences and Pathobiology, Virginia Maryland Regional College of Veterinary Medicine, Virginia-Tech and University of Maryland, Blacksburg, Virginia 24061, USASearch for more papers by this authorB. V. Troan, B. V. Troan Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorN. J. H. Sharp, N. J. H. Sharp Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USA Animal Critical Care Group, 1410 Boundary Road, Burnaby, British Columbia V5K 4V3, CanadaSearch for more papers by this authorN. B. Campbell, N. B. Campbell Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this authorC. F. Brownie, C. F. Brownie Department of Clinical Sciences, Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, North Carolina 27606, USASearch for more papers by this author First published: 05 January 2010 https://doi.org/10.1111/j.2042-3292.2005.tb00349.xCitations: 9 AboutPDF 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 onFacebookTwitterLinkedInRedditWechat Citing Literature Volume17, Issue3June 2005Pages 118-122 RelatedInformation}, number={3}, journal={Equine Veterinary Education}, author={Gardner, S. Y. and Cook, A. G. and Jortner, B. S. and Troan, B. V. and Sharp, N. J. H. and Campbell, N. B. and Brownie, C. F.}, year={2005}, pages={118–122} }
 @article{gardner_atkins_sams_schwabenton_papich_2004, title={Characterization of the Pharmacokinetic and Pharmacodynamic Properties of the Angiotensin-Converting Enzyme Inhibitor, Enalapril, in Horses}, volume={18}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/j.1939-1676.2004.tb00166.x}, DOI={10.1111/j.1939-1676.2004.tb00166.x}, abstractNote={The pharmacokinetics of enalapril (0.5 mg/kg IV) and the pharmacodynamics of enalapril (0.5 mg/kg PO) in 5 mares were investigated. After single IV dosing, concentrations of enalapril and enalaprilat, its active metabolite, were measured. Two weeks later, enalapril was administered by nasogastric tube. Potassium, creatinine, blood urea nitrogen (BUN), enalapril, and enalaprilat concentrations and angiotensin converting enzyme (ACE) activity were measured in serum. In addition, heart rate, blood pressure, digital venous blood gases, and lactate were measured. Two weeks later, enalapril was again administered by nasogastric tube. To mimic activation of the renin‐angiotensin‐aldosterone system, angiotensin I (0.5 μg/kg) was administered at fixed intervals, followed by blood‐pressure and heart‐rate measurement. The elimination half lives of enalapril and enalaprilat were 0.59 and 1.25 hours, respectively, after IV administration. After PO administration, enalapril and enalaprilat were not detectable in serum. There was a tendency(P= .0625) toward a decrease in ACE activity 45–120 minutes after enalapril administration, but ACE activity suppression was never >16%. There was a tendency(P= .0625) toward a decrease in mean arterial pressure (MAP) 6–8 hours after enalapril administration. Serum concentrations of potassium, creatinine, and BUN and digital venous blood gases and lactate concentrations did not change. In response to angiotensin I, there was a tendency(P= .0625) toward a decrease in the MAP response 4–24 hours after enalapril administration. Single‐dose enalapril at 0.5 mg/kg PO did not demonstrate significant availability, pharmacodynamic effect, or substantial suppression of ACE activity.}, number={2}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Gardner, Sarah Y. and Atkins, Clarke E. and Sams, Richard A. and Schwabenton, A. Brooke and Papich, Mark G.}, year={2004}, month={Mar}, pages={231–237} }
 @article{gardner_mcgee_kodavanti_ledbetter_everitt_winsett_doerfler_costa_2004, title={Emission-particle-induced ventilatory abnormalities in a rat model of pulmonary hypertension}, volume={112}, ISSN={["0091-6765"]}, DOI={10.1289/ehp.6583}, abstractNote={Preexistent cardiopulmonary disease in humans appears to enhance susceptibility to the adverse effects of ambient particulate matter. Previous studies in this laboratory have demonstrated enhanced inflammation and mortality after intratracheal instillation (IT) and inhalation (INH) of residual oil fly ash (ROFA) in a rat model of pulmonary hypertension induced by monocrotaline (MCT). The present study was conducted to examine the effects of ROFA in this model on ventilatory function in unanesthetized, unrestrained animals. Sixty-day-old male CD rats were injected with MCT (60 mg/kg) or vehicle (VEH) intraperitoneally 10 days before IT of ROFA (8.3 mg/kg) or saline (SAL) (control) or nose-only INH of ROFA [15 mg/m3 for 6 hr on 3 consecutive days or air (control)]. At 24 and 72 hr after exposure, rats were studied individually in a simultaneous gas uptake/whole-body plethysmograph. Lungs were removed at 72 hr for histology. Pulmonary test results showed that tidal volume (VT) decreased 24 hr after IT of ROFA in MCT-treated rats. Breathing frequency, minute volume (VE), and the ventilatory equivalent for oxygen increased in MCT- and VEH-treated rats 24 hr after IT or INH of ROFA and remained elevated 72 hr post-IT. O2 uptake (VO2) decreased after IT of ROFA in MCT-treated rats. Carbon monoxide uptake decreased 24 hr after IT of ROFA, returning to control values in VEH-treated rats but remaining low in MCT-treated rats 72 hr post-IT. ROFA exposure induced histologic changes and abnormalities in several ventilatory parameters, many of which were enhanced by MCT treatment.}, number={8}, journal={ENVIRONMENTAL HEALTH PERSPECTIVES}, author={Gardner, SY and McGee, JK and Kodavanti, UP and Ledbetter, A and Everitt, JI and Winsett, DW and Doerfler, DL and Costa, DL}, year={2004}, month={Jun}, pages={872–878} }
 @article{gardner_davis_jones_lafevers_hoskins_mcarver_papich_2004, title={Moxifloxacin pharmacokinetics in horses and disposition into phagocytes after oral dosing}, volume={27}, ISSN={["1365-2885"]}, url={http://europepmc.org/abstract/med/14995968}, DOI={10.1046/j.0140-7783.2003.00529.x}, abstractNote={Journal of Veterinary Pharmacology and TherapeuticsVolume 27, Issue 1 p. 57-60 Moxifloxacin pharmacokinetics in horses and disposition into phagocytes after oral dosing S. Y. Gardner, S. Y. Gardner Department of Clinical SciencesSearch for more papers by this authorJ. L. Davis, J. L. Davis Department of Clinical SciencesSearch for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical SciencesSearch for more papers by this authorD. H. LaFevers, D. H. LaFevers Department of Clinical SciencesSearch for more papers by this authorM. S. Hoskins, M. S. Hoskins Department of Clinical SciencesSearch for more papers by this authorE. M. Mcarver, E. M. Mcarver Department of Clinical SciencesSearch for more papers by this authorM. G. Papich, M. G. Papich Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this author S. Y. Gardner, S. Y. Gardner Department of Clinical SciencesSearch for more papers by this authorJ. L. Davis, J. L. Davis Department of Clinical SciencesSearch for more papers by this authorS. L. Jones, S. L. Jones Department of Clinical SciencesSearch for more papers by this authorD. H. LaFevers, D. H. LaFevers Department of Clinical SciencesSearch for more papers by this authorM. S. Hoskins, M. S. Hoskins Department of Clinical SciencesSearch for more papers by this authorE. M. Mcarver, E. M. Mcarver Department of Clinical SciencesSearch for more papers by this authorM. G. Papich, M. G. Papich Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USASearch for more papers by this author First published: 18 February 2004 https://doi.org/10.1046/j.0140-7783.2003.00529.xCitations: 28 Sarah Y. Gardner, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606, USA. E-mail: [email protected] Read 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 Citing Literature Volume27, Issue1February 2004Pages 57-60 RelatedInformation}, number={1}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Gardner, SY and Davis, JL and Jones, SL and Lafevers, DH and Hoskins, MS and Mcarver, M and Papich, MG}, year={2004}, month={Feb}, pages={57–60} }
 @article{johansson_gardner_levine_papich_lafevers_goldman_sheets_atkins_2004, title={Pharmacokinetics and pharmacodynamics of furosemide after oral administration to horses}, volume={18}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2004)18<739:PAPOFA>2.0.CO;2}, abstractNote={Furosemide is the most common diuretic drug used in horses. Furosemide is routinely administered as IV or IM bolus doses 3-4 times a day. Administration PO is often suggested as an alternative, even though documentation of absorption and efficacy in horses is lacking. This study was carried out in a randomized, crossover design and compared 8-hour urine volume among control horses that received placebo, horses that received furosemide at 1 mg/kg PO, and horses that received furosemide at 1 mg/kg IV. Blood samples for analysis of plasma furosemide concentrations, PCV, and total solids were obtained at specific time points from treated horses. Furosemide concentrations were determined by reversed-phase high-performance liquid chromatography with fluorescent detection. Systemic availability of furosemide PO was poor, erratic, and variable among horses. Median systemic bioavailability was 5.4% (25th percentile, 75th percentile: 3.5, 9.6). Horses that received furosemide IV produced 7.4 L (7.1, 7.7) of urine over the 8-hour period. The maximum plasma concentration of 0.03 microg/mL after administration PO was not sufficient to increase urine volume compared with control horses (1.2 L [1.0, 1.4] PO versus 1.2 L [1.0, 1.4] control). There was a mild decrease in urine specific gravity within 1-2 hours after administration of furosemide PO, and urine specific gravity was significantly lower in horses treated with furosemide PO compared with control horses at the 2-hour time point. Systemic availability of furosemide PO was poor and variable. Furosemide at 1 mg/kg PO did not induce diuresis in horses.}, number={5}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Levine, JF and Papich, MG and LaFevers, DH and Goldman, RB and Sheets, MK and Atkins, CE}, year={2004}, pages={739–743} }
 @article{johansson_gardner_levine_papich_lafevers_fuquay_reagan_atkins_2003, title={Furosemide continuous rate infusion in the horse: Evaluation of enhanced efficacy and reduced side effects}, volume={17}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2003)017<0887:FCRIIT>2.3.CO;2}, abstractNote={Journal of Veterinary Internal MedicineVolume 17, Issue 6 p. 887-895 Open Access Furosemide Continuous Rate Infusion in the Horse: Evaluation of Enhanced Efficacy and Reduced Side Effects Anna M. Johansson, Anna M. Johansson Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSarah Y. Gardner, Corresponding Author Sarah Y. Gardner Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, Department of Clinical Sciences, College of Veterinary Medicine, Hillsborough Street 4700, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorJay F. Levine, Jay F. Levine Department of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorMark G. Papich, Mark G. Papich Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorVirginia H. Reagan, Virginia H. Reagan Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this author Anna M. Johansson, Anna M. Johansson Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorSarah Y. Gardner, Corresponding Author Sarah Y. Gardner Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NC DVM, PhD, Department of Clinical Sciences, College of Veterinary Medicine, Hillsborough Street 4700, Raleigh, NC 27606; e-mail: [email protected].Search for more papers by this authorJay F. Levine, Jay F. Levine Department of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorMark G. Papich, Mark G. Papich Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorVirginia H. Reagan, Virginia H. Reagan Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this authorClarke E. Atkins, Clarke E. Atkins Department of Clinical Sciences College of Veterinary Medicine, North Carolina State University, Raleigh, NCSearch for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2003.tb02529.xCitations: 32AboutPDF 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 onEmailFacebookTwitterLinkedInRedditWechat Abstract Continuous rate infusion (CRI) of furosemide in humans is considered superior to intermittent administration (IA). This study examined whether furosemide CRI, compared with IA, would increase diuretic efficacy with decreased fluid and electrolyte fluctuations and activation of the renin-angiotensin-aldosterone system (RAAS) in the horse. Five mares were used in a crossover-design study. During a 24-hour period, each horse received a total of 3 mg/kg furosemide by either CRI (0.12 mg/kg/h preceded by a loading dose of 0.12 mg/kg IV) or IA (1 mg/kg IV q8h). There was not a statistically significant difference in urine volume over 24 hours between methods; however, urine volume was significantly greater after CRI compared with IA during the first 8 hours ([median 25th percentile, 75th percentile]: 9.6 L [8.9, 14.4] for CRI versus 5.9 L [5.3, 6.0] for IA). CRI produced a more uniform urine flow, decreased fluctuations in plasma volume, and suppressed renal concentrating ability throughout the infusion period. Potassium, Ca, and Cl excretion was greater during CRI than IA (1,133 mmol [1,110, 1,229] versus 764 mmol [709, 904], 102.7 mmol [96.0, 117.2] versus 73.3 mmol [65.0, 73.5], and 1,776 mmol [1,657, 2,378] versus 1,596 mmol [1,457, 1,767], respectively). Elimination half-lives of furosemide were 1.35 and 0.47 hours for CRI and IA, respectively. The area under the excretion rate curve was 1,285.7 and 184.2 mL mg/mL for CRI and IA, respectively. Furosemide CRI (0.12 mg/kg/h) for 8 hours, preceded by a loading dose (0.12 mg/kg), is recommended when profound diuresis is needed acutely in horses. References 1 Jackson EK. Diuretics. In: JG Hardman, LE Limbird, PB Molinoff, RW Ruddon, AG Gilman, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. New York , NY : The McGraw-Hills Companies; 1995: 685–715. Web of Science®Google Scholar 2 Rose BD. Diuretics. 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Web of Science®Google Scholar 21 Chennavasin P, Seiwell R, Brater DC, et al. Pharmacodynamic analysis of the furosemide-probenecid interaction in man. Kidney Int 1979; 16: 187–195. 10.1038/ki.1979.120 CASPubMedWeb of Science®Google Scholar 22 Kaojarern S, Day B, Brater DC. The time course of delivery of furosemide into urine: An independent determinant of overall response. Kidney Int 1982; 22: 69–74. 10.1038/ki.1982.134 CASPubMedWeb of Science®Google Scholar 23 Hammarlund MM, Odlind B, Paalzow LK. Acute tolerance to furosemide diuresis in humans. Pharmacokinetic-pharmacodynamic modeling. J Pharmacol Exp Ther 1985; 233: 447–453. CASPubMedWeb of Science®Google Scholar 24 Streeten DH, Tomycz N, Anderson GH. Reliability of screening methods for the diagnosis of primary aldosteronism. Am J Med 1979; 67: 403–413. 10.1016/0002-9343(79)90786-1 CASPubMedWeb of Science®Google Scholar 25 Roberts BL, Blake JW, Tobin T. The pharmacology of furose-mide in the horse. II. Its detection, pharmacokinetics, and clearance from urine. J Equine Med Surg 1978; 2: 185–194. CASWeb of Science®Google Scholar Citing Literature Volume17, Issue6November 2003Pages 887-895 ReferencesRelatedInformation}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Levine, JF and Papich, MG and LaFevers, DH and Fuquay, LR and Reagan, VH and Atkins, CE}, year={2003}, pages={887–895} }
 @article{johansson_gardner_jones_fuquay_reagan_levine_2003, title={Hypomagnesemia in hospitalized horses}, volume={17}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2003)017<0860:HIHH>2.3.CO;2}, abstractNote={This study was initiated to identify the signalment and clinical variables potentially associated with hypomagnesemia in horses evaluated at the North Carolina State University, College of Veterinary Medicine (NCSU-CVM) veterinary teaching hospital between January 1999 and May 2001. A nested case reference study (nested case-control study) was conducted to examine the potential relationship between hypomagnesemia and signalment, serum chemistry panel analyses, number of hospitalization days, discharge status, and diagnosis. A series of independent and multivariable logistic regression models were used to assess the potential association of each variable with low total serum magnesium concentrations. Four hundred one of 823 (48.7%) horses had serum total magnesium concentrations below the normal reference range. Hypomagnesemia was more likely to occur in horses older than 1 month of age. Colic (odds ratio [OR]: 2.96, 95% confidence intervals [CI]: 2.14–4.08), acute diarrhea (OR: 5.91, 95% CI: 2.32–15.06), other gastrointestinal disease (OR: 2.07, 95% CI: 1.15–3.71), infectious respiratory disease (OR: 5.07, 95% CI: 2.09–12.28), and multiorgan system disease (OR: 2.31, 95% CI: 1.24–4.28) were associated with hypomagnesemia in adult horses, whereas foals with diarrhea (excluding septic foals) (OR: 0.11, 95% CI: 0.01–0.84) were less likely to have hypomagne-semia. Overall, there was no relationship between hypomagnesemia and mortality (OR: 1.00, 95% CI: 0.72–1.41), but horses with colic and hypomagnesemia were less likely to die than horses with colic and normal or high total magnesium (OR: 0.53, 95% CI: 0.30–0.95). Among horses that survived, hypomagnesemia at admission was associated with a longer hospitalization period (OR: 1.45, 95% CI: 1.00–2.11).}, number={6}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Johansson, AM and Gardner, SY and Jones, SL and Fuquay, LR and Reagan, VH and Levine, JF}, year={2003}, pages={860–867} }
 @article{little_flowers_hammerberg_gardner_2003, title={Management of drug-resistant cyathostominosis on a breeding farm in central North Carolina}, volume={35}, ISSN={["2042-3306"]}, DOI={10.2746/042516403776148264}, abstractNote={Summary}, number={3}, journal={EQUINE VETERINARY JOURNAL}, author={Little, D and Flowers, JR and Hammerberg, BH and Gardner, SY}, year={2003}, month={May}, pages={246–251} }
 @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{davis_gardner_jones_schwabenton_papich_2002, title={Pharmacokinetics of azithromycin in foals after i.v. and oral dose and disposition into phagocytes}, volume={25}, ISSN={["1365-2885"]}, url={http://europepmc.org/abstract/med/12000529}, DOI={10.1046/j.1365-2885.2002.00387.x}, abstractNote={The properties of azithromycin suggest that it may be an alternative to erythromycin for treatment of Rhodococcus equi pneumonia in foals. To investigate this possibility, the disposition of azithromycin in plasma, polymorphonuclear leukocytes (PMN), and alveolar cells was examined after a single administration in foals. Azithromycin suspension was administered orally (p.o.) at a dose of 10 mg/kg to five healthy 2–3‐month‐old foals. Two weeks later, azithromycin for injection was administered by intravenous (i.v.) infusion at a dose of 5 mg/kg to the same foals. Plasma samples were collected after p.o. and i.v. administration. Peripheral blood PMN and bronchoalveolar lavage fluid and alveolar cells were collected after p.o. administration. Azithromycin concentrations were determined by reverse‐phase high‐performance liquid chromatography (HPLC) with coulometric electrochemical detection. Azithromycin p.o. absorption was variable with a mean systemic availability of 39% (±20%). The plasma half‐life was 16 and 18.3 h after i.v. and p.o. administration, respectively. Azithromycin had a very large volume of distribution (Vd) of 11.6 L/kg [Vd(ss)] and 12.4 L/kg [Vd(area)]. The large Vd can be attributed to high tissue and intracellular concentrations, exhibited by the high concentration of azithromycin in PMN and alveolar cells. The PMN half‐life was 49.2 h. Dosage of 10 mg/kg of azithromycin p.o. once daily for foals with R. equi pneumonia is recommended for further study.}, number={2}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Davis, JL and Gardner, SY and Jones, SL and Schwabenton, BA and Papich, MG}, year={2002}, month={Apr}, pages={99–104} }
 @article{gardner_papich_2001, title={Comparison of cefepime pharmacokinetics in neonatal foals and adult dogs}, volume={24}, ISSN={0140-7783 1365-2885}, url={http://dx.doi.org/10.1046/j.1365-2885.2001.00326.x}, DOI={10.1046/j.1365-2885.2001.00326.x}, abstractNote={The pharmacokinetics of cefepime, a new fourth generation cephalosporin with enhanced antibacterial activity, was examined in neonatal foals and adult dogs. Cefepime was administered intravenously (i.v.) at a dose of 14 mg/kg to five neonatal foals and six adult dogs. Blood samples were collected in both groups of animals and plasma cefepime concentrations measured by reverse‐phase high‐performance liquid chromatography (HPLC). Cefepime concentrations in both groups of animals were described by a two‐compartment pharmacokinetic model with elimination half‐lives of 1.65 and 1.09 h for the foal and dog, respectively. We tested whether or not pharmacokinetic parameters for cefepime could be scaled across species using principles of allometry. The parameters of elimination half‐life (t½β), apparent volume of distribution (VDarea), and systemic clearance (CL) were scaled linearly to body weight on a double logarithmic plot with allometric exponents for body weight of 0.26, 1.08 and 0.72, respectively. This study further determined doses for cefepime, a potentially useful antibiotic for neonatal foals and dogs, from the pharmacokinetic values. An i.v. dose of cefepime estimated from this study for treating sensitive bacteria was 11 mg/kg every 8 h for neonatal foals and 40 mg/kg every 6 h for dogs.}, number={3}, journal={Journal of Veterinary Pharmacology and Therapeutics}, publisher={Wiley}, author={Gardner, S. Y. and Papich, M. G.}, year={2001}, month={Jun}, pages={187–192} }
 @article{gardner_lehmann_costa_2000, title={Oil fly ash-induced elevation of plasma fibrinogen levels in rats}, volume={56}, ISSN={["1096-6080"]}, DOI={10.1093/toxsci/56.1.175}, abstractNote={Particulate matter air pollution (PM) has been associated with morbidity and mortality from ischemic heart disease and stroke in humans. It has been hypothesized that alveolar inflammation, resulting from exposure to PM, may induce a state of blood hypercoagulability, triggering cardiovascular events in susceptible individuals. Previous studies in our laboratory have demonstrated acute lung injury with alveolar inflammation in rats following exposure to residual oil fly ash (ROFA), an emission source particulate. In addition, increased mortality has been documented following exposure to ROFA in rats with preexistent cardiopulmonary disease. ROFA's toxicity derives from its soluble metal content, which appears also to drive the toxicity of ambient PM. The present study was conducted to test the hypothesis that exposure of rats to a toxic PM, like ROFA, would adversely alter hemostatic parameters and cardiovascular risk factors thought to be involved in human epidemiologic findings. Sixty-day-old male Sprague-Dawley rats were exposed by intratracheal instillation (IT) to varying doses (0.3, 1. 7, or 8.3 mg/kg) of ROFA, 8.3 mg/kg Mt. Saint Helen's volcanic ash (MSH, control particle), or 0.3 ml saline (SAL, control). At 24 h post-IT, activated partial thromboplastin time (APTT), prothrombin time (PT), plasma fibrinogen (PF), plasma viscosity (PV), and complete blood count (CBC) were performed on venous blood samples. No differences from control were detected in APTT and PT in ROFA-exposed rats; however, ROFA exposure did result in elevated PF, at 8.3 mg/kg only. In addition, PV values were elevated in both ROFA and MSH-exposed rats relative to SAL-control rats, but not significantly. Although no changes were detected in APTT and PT, alteration of important hematologic parameters (notably fibrinogen) through PM induction of an inflammatory response may serve as biomarkers of cardiovascular risk in susceptible individuals.}, number={1}, journal={TOXICOLOGICAL SCIENCES}, author={Gardner, SY and Lehmann, JR and Costa, DL}, year={2000}, month={Jul}, pages={175–180} }
 @article{kodavanti_jackson_ledbetter_richards_gardner_watkinson_campen_costa_1999, title={Lung injury from intratracheal and inhalation exposures to residual oil fly ash in a rat model of monocrotaline-induced pulmonary hypertension}, volume={57}, ISSN={["1087-2620"]}, DOI={10.1080/009841099157502}, abstractNote={A rat model of monocrotaline (MCT)-induced pulmonary injury/hypertension has been recently used in particulate matter (PM) health effects studies, however, results have been equivocal. Neither the mechanism by which mortality occurs in this model nor the variation in response due to differences in PM exposure protocols (i.e., a bolus dose delivered intratracheally versus a similar cumulative dose inhaled over three days) have been fully investigated. Sprague Dawley rats (SD, 60 d old; 250-300 g) were injected with either saline (healthy) or MCT, 60 mg/kg, i.p. (to induce pulmonary injury/hypertension). Ten days later they were exposed to residual oil fly ash (ROFA), either intratracheally (IT; saline, 0.83 or 3.33 mg/kg) or by nose-only inhalation (15 mg/m3 x 6 h/d x 3 d). Lung histology, pulmonary cytokine gene expression (0 and 18 h postinhalation), and bronchoalveolar lavage fluid (BALF) markers of injury were analyzed (24 and 96 h post-IT; or 18 h post-inhalation). Data comparisons examined three primary aspects, 1) ROFA IT versus inhalation effects in healthy rats; 2) pulmonary injury caused by MCT; and 3) exacerbation of ROFA effects in MCT rats. In the first aspect, pulmonary histological lesions following ROFA inhalation in healthy rats were characterized by edema, inflammatory cell infiltration, and thickening of alveolar walls. Increases in BALF markers of lung injury and inflammation were apparent in ROFA-IT or nose-only exposed healthy rats. Increased IL-6, and MIP-2 expression were also apparent in healthy rats following ROFA inhalation. In regards to the second aspect, MCT rats exposed to saline or air showed perivascular inflammatory cell infiltrates, increased presence of large macrophages, and alveolar thickening. Consistently, BALF protein, and inflammatory markers (macrophage and neutrophil counts) were elevated indicating pulmonary injury. In regards to the third aspect, 58% of MCT rats exposed to ROFA IT died within 96 h regardless of the dose. No mortality was observed using the inhalation protocol. ROFA inhalation in MCT rats caused exacerbation of lung lesions such as increased edema, alveolar wall thickening, and inflammatory cell infiltration. This exacerbation was also evident in terms of additive or more than additive increases in BALF neutrophils, macrophages and eosinophils. IL-6 but not MIP-2 expression was more than additive in MCT rats, and persisted over 18 h following ROFA. IL-10 and cellular fibronectin expression was only increased in MCT rats exposed to ROFA. In summary, only the bolus IT ROFA caused mortality in the rat model of lung injury/hypertension. Exacerbation of histological lesions and cytokine mRNA expression were most reflective of increased ROFA susceptibility in this model.}, number={8}, journal={JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES}, author={Kodavanti, UP and Jackson, MC and Ledbetter, AD and Richards, JR and Gardner, SY and Watkinson, WP and Campen, MJ and Costa, DL}, year={1999}, month={Aug}, pages={543–563} }
 @article{gardner_aucoin_1994, title={PHARMACOKINETICS OF CEFTRIAXONE IN MARES}, volume={17}, ISSN={["0140-7783"]}, DOI={10.1111/j.1365-2885.1994.tb00226.x}, abstractNote={Journal of Veterinary Pharmacology and TherapeuticsVolume 17, Issue 2 p. 155-156 Pharmacokinetics of ceftriaxone in mares S. Y. GARDNER, S. Y. GARDNER Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USASearch for more papers by this authorD. P. AUCOIN, D. P. AUCOIN Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USASearch for more papers by this author S. Y. GARDNER, S. Y. GARDNER Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USASearch for more papers by this authorD. P. AUCOIN, D. P. AUCOIN Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USASearch for more papers by this author First published: April 1994 https://doi.org/10.1111/j.1365-2885.1994.tb00226.xCitations: 16AboutPDF 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 onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume17, Issue2April 1994Pages 155-156 RelatedInformation}, number={2}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={GARDNER, SY and AUCOIN, DP}, year={1994}, month={Apr}, pages={155–156} }