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Author Nicol, C.J.; Adachi, M.; Akiyama, T.E.; Gonzalez, F.J.
Title PPARgamma in endothelial cells influences high fat diet-induced hypertension Type Journal Article
Year 2005 Publication American journal of hypertension : journal of the American Society of Hypertension Abbreviated Journal Am J Hypertens
Volume 18 Issue 4 Pt 1 Pages 549-556
Keywords Administration, Oral; Animals; Antihypertensive Agents/pharmacology; Blood Pressure/drug effects; Diabetes Mellitus, Type 2/physiopathology; Dietary Fats/*administration & dosage/pharmacology; Dose-Response Relationship, Drug; Endothelial Cells/*metabolism; Female; Heart Rate/drug effects; Hypertension/*etiology; Ligands; Male; Mice; Mice, Knockout; PPAR gamma/*metabolism; Sodium Chloride/administration & dosage/pharmacology; Thiazolidinediones/pharmacology
Abstract BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands improve human hypertension. However, the mechanism and site of this effect remains unknown, confounded by PPARgamma expression in many cell types, including endothelial cells (ECs). METHODS: To evaluate the vascular role of PPARgamma we used a conditional null mouse model. Specific disruption of PPARgamma in ECs was created by crossing Tie2-Cre+ transgenic (T2T+) and PPARgamma-floxed (fl/fl) mice to generate PPARgamma (fl/fl)T2T+ (PPARgamma E-null) mice. Conscious 8- to 12-week-old congenic PPARgamma (fl/fl)Cre- (wild type) and PPARgamma E-null mice were examined for changes in systolic blood pressure (BP) and heart rate (HR), untreated, after 2 months of salt-loading (drinking water), and after treatment for 3 months with high fat (HF) diet alone or supplemented during the last 2 weeks with rosiglitazone (3 mg/kg/d). RESULTS: Untreated PPARgamma E-nulls were phenotypically indistinguishable from wild-type littermates. However, compared to similarly treated wild types, HF-treated PPARgamma E-nulls had significantly elevated systolic BP not seen after normal diet or salt-loading. Despite sex-dependent baseline differences, salt-loaded and HF-treated PPARgamma E-nulls of either sex had significantly elevated HR versus wild types. Interestingly, rosiglitazone improved serum insulin levels, but not HF diet-induced hypertension, in PPARgamma E-null mice. CONCLUSIONS: These results suggest that PPARgamma in ECs not only is an important regulator of hypertension and HR under stressed conditions mimicking those arising in type 2 diabetics, but also mediates the antihypertensive effects of rosiglitazone. These data add evidence supporting a beneficial role for PPARgamma-specific ligands in the treatment of hypertension, and suggest therapeutic strategies targeting ECs may prove useful.
Address Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0895-7061 ISBN Medium
Area Expedition Conference
Notes PMID:15831367 Approved no
Call Number refbase @ user @ Serial 69
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Author Jeong, S.; Han, M.; Lee, H.; Kim, M.; Kim, J.; Nicol, C.J.; Kim, B.H.; Choi, J.H.; Nam, K.-H.; Oh, G.T.; Yoon, M.
Title Effects of fenofibrate on high-fat diet-induced body weight gain and adiposity in female C57BL/6J mice Type Journal Article
Year 2004 Publication Metabolism: clinical and experimental Abbreviated Journal Metabolism
Volume 53 Issue 10 Pages 1284-1289
Keywords Adipose Tissue/*anatomy & histology/drug effects; Animals; Antilipemic Agents/*pharmacology; Body Composition/*drug effects; Body Weight/drug effects; Dietary Fats/*pharmacology; Eating/drug effects; Fatty Acids/metabolism; Female; Gene Expression Regulation/drug effects; Leptin/metabolism; Liver/metabolism; Mice; Mice, Inbred C57BL; Ovariectomy; Procetofen/*pharmacology; RNA, Messenger/biosynthesis/genetics; Receptors, Cytoplasmic and Nuclear/biosynthesis/genetics/metabolism; Transcription Factors/biosynthesis/genetics/metabolism; Weight Gain/*drug effects
Abstract Our previous study suggested that fenofibrate affects obesity and lipid metabolism in a sexually dimorphic manner in part through the differential activation of hepatic peroxisome proliferator-activated receptor alpha (PPARalpha) in male and female C57BL/6J mice. To determine whether fenofibrate reduces body weight gain and adiposity in female sham-operated (Sham) and ovariectomized (OVX) C57BL/6J mice, the effects of fenofibrate on not only body weight, white adipose tissue (WAT) mass, and food intake, but also the expression of both leptin and PPARalpha target genes were measured. Compared to their respective low-fat diet-fed controls, both Sham and OVX mice exhibited increases in body weight and WAT mass when fed a high-fat diet. Fenofibrate treatment decreased body weight gain and WAT mass in OVX, but not in Sham mice. Furthermore, fenofibrate increased the mRNA levels of PPARalpha target genes encoding peroxisomal enzymes involved in fatty acid beta-oxidation, and reduced apolipoprotein C-III (apo C-III) mRNA, all of which were expressed at higher levels in OVX compared to Sham mice. However, leptin mRNA levels were found to positively correlate with WAT mass, and food intake was not changed in either OVX or Sham mice following fenofibrate treatment. These results suggest that fenofibrate differentially regulates body weight and adiposity due in part to differences in PPARalpha activation, but not to differences in leptin production, between female OVX and Sham mice.
Address Department of Life Sciences, Mokwon University, Taejon, Korea
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0026-0495 ISBN Medium
Area Expedition Conference
Notes PMID:15375783 Approved no
Call Number refbase @ user @ Serial 72
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Author Crosby, M.B.; Svenson, J.L.; Zhang, J.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S.
Title Peroxisome proliferation-activated receptor (PPAR)gamma is not necessary for synthetic PPARgamma agonist inhibition of inducible nitric-oxide synthase and nitric oxide Type Journal Article
Year 2005 Publication The Journal of pharmacology and experimental therapeutics Abbreviated Journal J Pharmacol Exp Ther
Volume 312 Issue 1 Pages 69-76
Keywords Animals; Cell Line; Gene Expression/drug effects; Macrophages/drug effects/metabolism; Mice; Mice, Inbred C57BL; Nitric Oxide/*metabolism; Nitric Oxide Synthase/*metabolism; Nitric Oxide Synthase Type II; PPAR delta/metabolism; PPAR gamma/*agonists/deficiency; Thiazolidinediones/pharmacology
Abstract Peroxisome proliferation-activated receptor (PPAR)gamma agonists inhibit inducible nitric-oxide synthase (iNOS), tumor necrosis factor-alpha, and interleukin-6. Because of these effects, synthetic PPARgamma agonists, including thiazolidinediones, are being studied for their impact on inflammatory disease. The anti-inflammatory concentrations of synthetic PPARgamma agonists range from 10 to 50 microM, whereas their binding affinity for PPARgamma is in the nanomolar range. The specificity of synthetic PPARgamma agonists for PPARgamma at the concentrations necessary for anti-inflammatory effects is thus in question. We report that PPARgamma is not necessary for the inhibition of iNOS by synthetic PPARgamma agonists. RAW 264.7 macrophages possess little PPARgamma, yet lipopolysaccharide (LPS)/interferon (IFN)gamma-induced iNOS was inhibited by synthetic PPARgamma agonists at 20 microM. Endogenous PPARgamma was inhibited by the transfection of a dominant-negative PPARgamma construct into murine mesangial cells. In the transfected cells, synthetic PPARgamma agonists inhibited iNOS production at 10 microM, similar to nontransfected cells. Using cells from PPARgamma Cre/lox conditional knockout mice, baseline and LPS/IFNgamma-induced nitric oxide levels were higher in macrophages lacking PPARgamma versus controls. However, synthetic PPARgamma agonists inhibited iNOS at 10 microM in the PPARgamma-deficient cells, similar to macrophages from wild-type mice. These results indicate that PPARgamma is not necessary for inhibition of iNOS expression by synthetic PPARgamma agonists at concentrations over 10 microM. Intrinsic PPARgamma function, in the absence of synthetic agonists, however, may play a role in inflammatory modulation.
Address Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0022-3565 ISBN Medium
Area Expedition Conference
Notes PMID:15356214 Approved no
Call Number refbase @ user @ Serial 73
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Author Cheung, C.; Akiyama, T.E.; Ward, J.M.; Nicol, C.J.; Feigenbaum, L.; Vinson, C.; Gonzalez, F.J.
Title Diminished hepatocellular proliferation in mice humanized for the nuclear receptor peroxisome proliferator-activated receptor alpha Type Journal Article
Year 2004 Publication Cancer research Abbreviated Journal Cancer Res
Volume 64 Issue 11 Pages 3849-3854
Keywords Animals; Anticholesteremic Agents/pharmacology; Carcinogens/pharmacology; Cell Division; DNA Replication/drug effects; Fatty Acids/metabolism; Hepatocytes/cytology/drug effects/metabolism/*physiology; Humans; Mice; Mice, Transgenic; Oxidation-Reduction; Peroxisome Proliferators/pharmacology; Pyrimidines/pharmacology; Receptors, Cytoplasmic and Nuclear/genetics/*physiology; Species Specificity; Transcription Factors/genetics/*physiology
Abstract Lipid-lowering fibrate drugs function as agonists for the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha). Sustained activation of PPARalpha leads to the development of liver tumors in rats and mice. However, humans appear to be resistant to the induction of peroxisome proliferation and the development of liver cancer by fibrate drugs. The molecular basis of this species difference is not known. To examine the mechanism determining species differences in peroxisome proliferator response between mice and humans, a PPARalpha-humanized mouse line was generated in which the human PPARalpha was expressed in liver under control of the tetracycline responsive regulatory system. The PPARalpha-humanized and wild-type mice responded to treatment with the potent PPARalpha ligand Wy-14643 as revealed by induction of genes encoding peroxisomal and mitochondrial fatty acid metabolizing enzymes and resultant decrease of serum triglycerides. However, surprisingly, only the wild-type mice and not the PPARalpha-humanized mice exhibited hepatocellular proliferation as revealed by elevation of cell cycle control genes, increased incorporation of 5-bromo-2'-deoxyuridine into hepatocyte nuclei, and hepatomegaly. These studies establish that following ligand activation, the PPARalpha-mediated pathways controlling lipid metabolism are independent from those controlling the cell proliferation pathways. These findings also suggest that structural differences between human and mouse PPARalpha are responsible for the differential susceptibility to the development of hepatocarcinomas observed after treatment with fibrates. The PPARalpha-humanized mice should serve as models for use in drug development and human risk assessment and to determine the mechanism of hepatocarcinogenesis of peroxisome proliferators.
Address Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0008-5472 ISBN Medium
Area Expedition Conference
Notes PMID:15172993 Approved no
Call Number refbase @ user @ Serial 74
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Author Nicol, C.J.
Title Development, direction, and damage limitation: social learning in domestic fowl Type Journal Article
Year 2004 Publication Learning & behavior : a Psychonomic Society publication Abbreviated Journal Learn Behav
Volume 32 Issue 1 Pages 72-81
Keywords Adaptation, Psychological; Age Factors; Animals; Behavior, Animal; *Chickens; *Feeding Behavior; *Food Preferences; *Imitative Behavior; Imprinting (Psychology); *Learning; Maternal Behavior; Reinforcement (Psychology); *Social Environment; *Social Facilitation
Abstract This review highlights two areas of particular interest in the study of social learning in fowl. First, the role of social learning in the development of feeding and foraging behavior in young chicks and older birds is described. The role of the hen as a demonstrator and possible teacher is considered, and the subsequent social influence of brood mates and other companions on food avoidance and food preference learning is discussed. Second, the way in which work on domestic fowl has contributed to an understanding of the importance of directed social learning is examined. The well-characterized hierarchical social organization of small chicken flocks has been used to design studies which demonstrate that the probability of social transmission is strongly influenced by social relationships between birds. The practical implications of understanding the role of social learning in the spread of injurious behaviors in this economically important species are briefly considered.
Address Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol, England. c.j.nicol@bristol.ac.uk
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1543-4494 ISBN Medium
Area Expedition Conference
Notes PMID:15161142 Approved no
Call Number refbase @ user @ Serial 75
Permanent link to this record
 

 
Author Albentosa, M.J.; Kjaer, J.B.; Nicol, C.J.
Title Strain and age differences in behaviour, fear response and pecking tendency in laying hens Type Journal Article
Year 2003 Publication British poultry science Abbreviated Journal Br Poult Sci
Volume 44 Issue 3 Pages 333-344
Keywords Age Factors; Aggression/*physiology; Animal Husbandry; Animals; *Behavior, Animal; Breeding; Chickens/genetics/*physiology; Fear/*physiology; Feathers/*injuries; Female; Housing, Animal; Population Density; Social Behavior
Abstract 1. Behaviours associated with a high or low tendency to feather peck could be used as predictors of feather pecking behaviour in selective breeding programmes. This study investigated how strain and age at testing influenced responses in behavioural tests. 2. Four layer-type strains (ISA Brown, Columbian Blacktail, Ixworth and a high feather pecking (HP) and a low feather pecking (LP) line of White Leghorn) were reared in 6 same-strain/line pens of 8 birds from one day old. Birds in half the pens were given an open field test, a novel object test and a test with loose feather bundles between 4 and 12 weeks of age and a tonic immobility (TI) test at 13 weeks of age. All pens were tested with fixed feather bundles at 26 weeks, and undisturbed behaviour in the home pens was videoed at 1 and 27 weeks of age. Daily records of plumage damage were used as an indicator of feather pecking activity in the home pens. 3. Strain did not influence novel object test, open field test or loose feather test behaviour, although age effects in all three tests indicated a reduction in fearfulness and/or an increase in exploratory behaviour with increasing age. 4. White Leghorns showed longer TI durations than the other strains but less pecking at fixed feather bundles than ISA Browns and Columbian Blacktails. 5. There were few associations between behaviour in the 5 different tests, indicating that birds did not have overall behavioural traits that were consistent across different contexts. This suggests hens cannot easily be categorised into different behavioural 'types', based on their test responses and casts doubt on the usefulness of tests as predictors of feather pecking.
Address Centre for Behavioural Biology, Division of Farm Animal Science, University of Bristol, Langford, Bristol, England. MAlbentosa@lincoln.ac.uk
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0007-1668 ISBN Medium
Area Expedition Conference
Notes PMID:13677322 Approved no
Call Number refbase @ user @ Serial 80
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Author Doherty, T.J.; Frazier, D.L.
Title Effect of intravenous lidocaine on halothane minimum alveolar concentration in ponies Type Journal Article
Year 1998 Publication Equine veterinary journal Abbreviated Journal Equine Vet J
Volume 30 Issue 4 Pages 300-303
Keywords Anesthetics/administration & dosage/blood/*pharmacology; Anesthetics, Inhalation/administration & dosage/*analysis; Animals; Consciousness/drug effects; Dose-Response Relationship, Drug; Halothane/administration & dosage/*analysis; Horses/*physiology; Infusions, Intravenous/veterinary; Lidocaine/administration & dosage/blood/*pharmacology; Male
Abstract This study investigated the effect of lidocaine i.v. on halothane minimum alveolar concentration (MAC) in ponies. Six ponies were anaesthetised with thiopentone and succinylcholine, intubated and anaesthesia maintained with halothane. Ventilation was controlled and blood pressure maintained within clinically acceptable limits. Following a 2 h equilibration period, baseline halothane MAC was determined. The ponies were then given a loading dose of lidocaine (2.5 or 5 mg/kg bwt) or saline over 5 min, followed by a constant infusion of lidocaine (50 or 100 microg/kg/min, or saline, respectively). The halothane MAC was redetermined after a 60 min infusion of lidocaine or saline. The baseline halothane MAC for the control group was mean +/- s.d. 0.94 +/- 0.03%, and no significant decrease occurred following saline infusion. Lidocaine decreased halothane MAC in a dose-dependent fashion (r = 0.86; P < 0.0003). The results indicate that i.v. lidocaine may have a role in equine anaesthesia.
Address Department of Large Animal Clinical Sciences, University of Tennessee, College of Veterinary Medicine, Knoxville 37901-1071, USA
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0425-1644 ISBN Medium
Area Expedition Conference
Notes PMID:9705112 Approved no
Call Number refbase @ user @ Serial 95
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Author Carroll, G.L.; Matthews, N.S.; Hartsfield, S.M.; Slater, M.R.; Champney, T.H.; Erickson, S.W.
Title The effect of detomidine and its antagonism with tolazoline on stress-related hormones, metabolites, physiologic responses, and behavior in awake ponies Type Journal Article
Year 1997 Publication Veterinary surgery : VS : the official journal of the American College of Veterinary Surgeons Abbreviated Journal Vet Surg
Volume 26 Issue 1 Pages 69-77
Keywords Adrenergic alpha-Antagonists/administration & dosage/*pharmacology; Animals; Behavior, Animal/drug effects/physiology; Blood Glucose/metabolism; Blood Pressure/drug effects/physiology; Consciousness/physiology; Dose-Response Relationship, Drug; Drug Interactions; Epinephrine/blood; Fatty Acids, Nonesterified/blood; Female; Heart Rate/drug effects/physiology; Horse Diseases/metabolism/physiopathology/psychology; Horses/blood/metabolism/*physiology; Hydrocortisone/blood; Hypnotics and Sedatives/administration & dosage/*pharmacology; Imidazoles/administration & dosage/*pharmacology; Injections, Intravenous; Male; Norepinephrine/blood; Receptors, Adrenergic, alpha/drug effects/*physiology; Stress/metabolism/physiopathology/veterinary; Time Factors; Tolazoline/administration & dosage/*pharmacology
Abstract Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [i.v.]) followed 20 minutes later by either tolazoline (4.0 mg/kg i.v.) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes before detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by cortisol, glucose, and free fatty acids. If antagonism of an alpha-agonist is contemplated, the potential effect on hormones and metabolites should be considered.
Address Department of Small Animal Medicine and Surgery, Texas A&M University, College Station, USA
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0161-3499 ISBN Medium
Area Expedition Conference
Notes PMID:9123816 Approved no
Call Number refbase @ user @ Serial 96
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Author Grubb, T.L.; Foreman, J.H.; Benson, G.J.; Thurmon, J.C.; Tranquilli, W.J.; Constable, P.D.; Olson, W.O.; Davis, L.E.
Title Hemodynamic effects of calcium gluconate administered to conscious horses Type Journal Article
Year 1996 Publication Journal of veterinary internal medicine / American College of Veterinary Internal Medicine Abbreviated Journal J Vet Intern Med
Volume 10 Issue 6 Pages 401-404
Keywords Animals; Blood Pressure/drug effects/physiology; Calcium/blood; Calcium Gluconate/administration & dosage/*pharmacology; Cardiac Output/drug effects/physiology; Consciousness/*physiology; Dose-Response Relationship, Drug; Female; Heart Rate/drug effects/physiology; Hemodynamic Processes/*drug effects/physiology; Horses/blood/*physiology; Infusions, Intravenous; Male; Myocardial Contraction/drug effects/physiology; Respiration/drug effects/physiology; Stroke Volume/drug effects/physiology; Time Factors
Abstract Calcium gluconate was administered to conscious horses at 3 different rates (0.1, 0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dtmax). Mean arterial pressure and right atrial pressure were unchanged; heart rate decreased markedly during calcium administration. Ionized calcium concentration remained between 54% and 57% of total calcium concentration throughout the study. We conclude that calcium gluconate can safely be administered to conscious horses at 0.1 to 0.4 mg/kg/min and that administration will result in improved cardiac function.
Address Department of Veterinary Clinical Medicine, University of Illinois at Urbana-Champaign, USA
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0891-6640 ISBN Medium
Area Expedition Conference
Notes PMID:8947873 Approved no
Call Number refbase @ user @ Serial 97
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Author Trim, C.M.; Moore, J.N.; Clark, E.S.
Title Renal effects of dopamine infusion in conscious horses Type Journal Article
Year 1989 Publication Equine veterinary journal. Supplement Abbreviated Journal Equine Vet J Suppl
Volume Issue 7 Pages 124-128
Keywords Animals; Blood Pressure/drug effects/physiology; Consciousness/*physiology; Creatinine/blood; Dopamine/administration & dosage/*pharmacology; Dose-Response Relationship, Drug; Female; Heart Rate/drug effects/physiology; Horses/*physiology; Infusions, Intravenous/veterinary; Kidney/blood supply/*drug effects/physiology; Osmolar Concentration; Potassium/blood; Random Allocation; Regional Blood Flow/drug effects/physiology; Renal Artery/drug effects/physiology/ultrasonography; Sodium/blood; Time Factors; Ultrasonography/methods/veterinary; Urination/physiology
Abstract An ultrasonic flow probe was implanted around a branch of the left renal artery in five horses. The effects of dopamine were studied in the unsedated horses 10 days after surgery. Three experiments, separated by at least two days, were performed in random order on each horse. In two experiments, dopamine was infused intravenously for 60 mins at either 2.5 and 5.0 micrograms/kg bodyweight (bwt)/min. Saline was infused for 60 mins before and after each infusion, and for 180 mins in the third experiment as a control. Renal blood flow increased during administration of dopamine at both dose rates (P = 0.0001). Urine volume increased (P = 0.055), and osmolality decreased (P < 0.05), with infusion of dopamine at 5.0 micrograms/kg bwt/min. Arterial blood pressure and heart rate were not significantly affected. Fractional excretions of sodium and potassium were not significantly changed with dopamine infusion. The higher dopamine dose rate was accompanied by dysrhythmias in some horses.
Address Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens 30602, USA
Corporate Author Thesis
Publisher (down) Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN ISBN Medium
Area Expedition Conference
Notes PMID:9118094 Approved no
Call Number refbase @ user @ Serial 99
Permanent link to this record