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Author Seyfarth, R.M.; Cheney, D.L. url  doi
openurl 
  Title Social cognition Type Journal Article
  Year 2015 Publication Animal Behaviour Abbreviated Journal  
  Volume 103 Issue Pages 191-202  
  Keywords evolution; fitness; future research; personality; selective pressure; skill; social cognition  
  Abstract The social intelligence hypothesis argues that competition and cooperation among individuals have shaped the evolution of cognition in animals. What do we mean by social cognition? Here we suggest that the building blocks of social cognition are a suite of skills, ordered roughly according to the cognitive demands they place upon individuals. These skills allow an animal to recognize others by various means; to recognize and remember other animals' relationships; and, perhaps, to attribute mental states to them. Some skills are elementary and virtually ubiquitous in the animal kingdom; others are more limited in their taxonomic distribution. We treat these skills as the targets of selection, and assume that more complex levels of social cognition evolve only when simpler methods are inadequate. As a result, more complex levels of social cognition indicate greater selective pressures in the past. The presence of each skill can be tested directly through field observations and experiments. In addition, the same methods that have been used to compare social cognition across species can also be used to measure individual differences within species and to test the hypothesis that individual differences in social cognition are linked to differences in reproductive success.  
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  Series Volume Series Issue Edition  
  ISSN 0003-3472 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number (up) Equine Behaviour @ team @ Serial 6025  
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Author Broekhuis, F.; Madsen, E.K.; Klaassen, B. url  doi
openurl 
  Title Predators and pastoralists: how anthropogenic pressures inside wildlife areas influence carnivore space use and movement behaviour Type Journal Article
  Year 2019 Publication Animal Conservation Abbreviated Journal Anim Conserv  
  Volume Issue Pages  
  Keywords cheetah; livestock; movement; human pressure; protected areas; space use  
  Abstract Abstract Across the globe, wildlife populations and their behaviours are negatively impacted by people. Protected areas are believed to be an antidote to increasing human pressures but even they are not immune to the impact of anthropogenic activities. Areas that have been set aside for the protection of wildlife therefore warrant more attention when investigating the impact of anthropogenic pressures on wildlife. We use cheetahs Acinonyx jubatus as a case study to explore how a large carnivore responds to anthropogenic pressures inside wildlife areas. Using GPS-collar data we investigate cheetah space use, both when moving and stationary, and movement parameters (speed and turn angles) in relation to human disturbance, distance to human settlement, livestock abundance and livestock site use inside wildlife areas. Space use was negatively influenced by human disturbance, resulting in habitat loss and fragmentation and potentially reducing landscape permeability between neighbouring wildlife areas. Cheetahs were also less likely to stop in areas where livestock numbers were high, but more likely to stop in areas that were frequently used by livestock. The latter could reflect that cheetahs are attracted to livestock however, cheetahs in the study area rarely predated on livestock. It is therefore more likely that areas that are frequently used by livestock attract wild herbivores, which in turn could influence cheetah space use. We did not find any effects of people and livestock on cheetahs? speed and turn angles which might be related to the resolution of the data. We found that cheetahs are sensitive to human pressures and we believe that they could be an indicator species for other large carnivores facing similar challenges. We suggest that further research is needed to determine the levels of anthropogenic pressures needed to maintain ecological integrity, especially inside wildlife areas.  
  Address  
  Corporate Author Thesis  
  Publisher John Wiley & Sons, Ltd (10.1111) Place of Publication Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1367-9430 ISBN Medium  
  Area Expedition Conference  
  Notes doi: 10.1111/acv.12483 Approved no  
  Call Number (up) Equine Behaviour @ team @ Serial 6522  
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Author Ahrendt, L.P.; Labouriau, R.; Malmkvist, J.; Nicol, C.J.; Christensen, J.W. url  doi
openurl 
  Title Development of a standard test to assess negative reinforcement learning in horses Type Journal Article
  Year 2015 Publication Applied Animal Behaviour Science Abbreviated Journal Appl. Anim. Behav. Sci.  
  Volume 169 Issue Pages 38-42  
  Keywords Algometry; Horse behaviour; Learning performance; Operant conditioning; Pressure-release; Horse training  
  Abstract Most horses are trained by negative reinforcement. Currently, however, no standardised test for evaluating horses' negative reinforcement learning ability is available. The aim of this study was to develop an objective test to investigate negative reinforcement learning in horses. Twenty-four Icelandic horses (3 years old) were included in this study. The horses were tested in a pressure-release task on three separate days with 10, 7 and 5 trials on each side, respectively. Each trial consisted of pressure being applied on the hindquarter with an algometer. The force of the pressure was increased until the horse moved laterally away from the point of pressure. There was a significant decrease in required force over trials on the first test day (P<0.001), but not the second and third day. The intercepts on days 2 and 3 differed significantly from day 1 (P<0.001), but not each other. Significantly stronger force was required on the right side compared to the left (P<0.001), but there was no difference between first and second side tested (P=0.56). Individual performance was evaluated by median-force and the change in force over trials on the first test day. These two measures may explain different characteristics of negative reinforcement learning. In conclusion, this study presents a novel, standardised test for evaluating negative reinforcement learning ability in horses.  
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  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0168-1591 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number (up) Equine Behaviour @ team @ Serial 6650  
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Author Youket, R.J.; Carnevale, J.M.; Houpt, K.A.; Houpt, T.R. openurl 
  Title Humoral, hormonal and behavioral correlates of feeding in ponies: the effects of meal frequency Type Journal Article
  Year 1985 Publication Journal of animal science Abbreviated Journal J. Anim Sci.  
  Volume 61 Issue 5 Pages 1103-1110  
  Keywords Animals; Behavior, Animal/physiology; Blood Glucose/*analysis; Blood Proteins/*analysis; Blood Volume; *Eating; Feeding Behavior/physiology; Female; Heart Rate; Horses/blood/*physiology; Male; Osmolar Concentration; Osmotic Pressure; Triiodothyronine/*blood  
  Abstract The effect of meal frequency on body fluid, glucose, triiodothyronine (T3), heart rate and behavior was measured in 10 ponies. A simple reversal design was used in which each pony received one meal/day (1X) for 2 wk and six meals/day (6X) for 2 wk. The total intake/day was held constant. Feeding was followed by a rise in plasma levels of glucose, T3, protein and osmolality. One large meal was followed by significantly greater changes in all of the variables than was a meal one-sixth the size. Plasma T3 rose from 41 +/- 5 (SE) ng/liter before feeding to 43 +/- 5 ng/liter following a small meal, but rose significantly higher, from 39 +/- 4 to 60 +/- 10 ng/liter, following a large meal. Glucose rose from 84 +/- 3 to 109 +/- 7 mg/dl following a small meal and rose significantly higher, from 83 +/- 3 to 154 +/- 11 mg/dl, after a large meal. Plasma protein rose from 6.55 +/- .14 to 6.62 +/- .16 g/dl following a small meal and from 6.45 +/- .14 to 6.99 +/- .11 g/dl following a large meal. Osmolality rose from 227 +/- 1 mosmol/liter before to 279 +/- 1 mosmol/liter following a small meal and significantly higher from 278 +/- 2 to 285 +/- 1 mosnol/liter following a large meal. Heart rate rose from 42 beats/min in the absence of feed to 50 beats/min when food was visible to the ponies and did not rise higher when eating began. There were no significant differences in the cardiac response to one large meal and that to a small meal.(ABSTRACT TRUNCATED AT 250 WORDS)  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0021-8812 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:4077755 Approved no  
  Call Number (up) refbase @ user @ Serial 51  
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Author Sufit, E.; Houpt, K.A.; Sweeting, M. openurl 
  Title Physiological stimuli of thirst and drinking patterns in ponies Type Journal Article
  Year 1985 Publication Equine veterinary journal Abbreviated Journal Equine Vet J  
  Volume 17 Issue 1 Pages 12-16  
  Keywords Animals; Blood Proteins/analysis; Drinking Behavior/drug effects/*physiology; Furosemide/pharmacology; Horses/*physiology; Male; Osmolar Concentration; Osmotic Pressure; Sodium Chloride/pharmacology; Thirst/drug effects/*physiology; Time Factors; Water Deprivation/physiology  
  Abstract The stimuli that elicit thirst were studied in four ponies. Nineteen hours of water deprivation produced an increase in plasma protein from 67 +/- 0.1 g/litre to 72 +/- 2 g/litre, a mean (+/- se) increase in plasma sodium from 139 +/- 3 to 145 +/- 2 mmol/litre and an increase in plasma osmolality from 297 +/- 1 to 306 +/- 2 mosmol/litre. Undeprived ponies drank 1.5 +/- 0.9 kg/30 mins; 19 h deprived ponies drank 10.2 +/- 2.5 kg/30 mins and corrected the deficits in plasma protein, plasma sodium and plasma osmolality as well as compensating for the water they would have drunk during the deprivation period. In order to determine if an increase in plasma osmolality would stimulate thirst, 250 ml of 15 per cent sodium chloride was infused intravenously. The ponies drank when osmolality increased 3 per cent and when plasma sodium rose from 136 +/- 3 mmol/litre to 143 +/- 3 mmol/litre. Ponies infused with 15 per cent sodium chloride drank 2.9 +/- 0.7 kg; those infused with 0.9 per cent sodium chloride drank 0.7 +/- 0.5 kg. In order to determine if a decrease in plasma volume would stimulate thirst, ponies were injected with 1 or 2 mg/kg bodyweight (bwt) frusemide. Plasma protein rose from 68 +/- 2 g/litre pre-injection to 75 +/- 2 g/litre 1 h after 1 mg/kg bwt frusemide and to 81 +/- 1 g/litre 1 h after 2 mg/kg bwt frusemide.(ABSTRACT TRUNCATED AT 250 WORDS)  
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  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0425-1644 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:3979367 Approved no  
  Call Number (up) refbase @ user @ Serial 56  
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Author Nicol, C.J.; Adachi, M.; Akiyama, T.E.; Gonzalez, F.J. doi  openurl
  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  
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  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 (up) refbase @ user @ Serial 69  
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Author Guo, G.L.; Moffit, J.S.; Nicol, C.J.; Ward, J.M.; Aleksunes, L.A.; Slitt, A.L.; Kliewer, S.A.; Manautou, J.E.; Gonzalez, F.J. doi  openurl
  Title Enhanced acetaminophen toxicity by activation of the pregnane X receptor Type Journal Article
  Year 2004 Publication Toxicological sciences : an official journal of the Society of Toxicology Abbreviated Journal Toxicol Sci  
  Volume 82 Issue 2 Pages 374-380  
  Keywords Acetaminophen/pharmacokinetics/*toxicity; Analgesics, Non-Narcotic/pharmacokinetics/*toxicity; Animals; Aryl Hydrocarbon Hydroxylases/biosynthesis; Biotransformation; Blotting, Northern; Chromatography, High Pressure Liquid; Cytochrome P-450 CYP3A; Membrane Proteins; Mice; Mice, Knockout; Oxidoreductases, N-Demethylating/biosynthesis; Pregnenolone Carbonitrile/pharmacology; Receptors, Cytoplasmic and Nuclear/*drug effects; Receptors, Steroid/*drug effects; Sulfhydryl Compounds/metabolism  
  Abstract The pregnane X receptor (PXR) is a ligand-activated transcription factor and member of the nuclear receptor superfamily. Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Therefore, it was hypothesized that activation of PXR plays a major role in APAP-induced hepatotoxicity. Pretreatment with the PXR activator, pregnenolone 16alpha-carbonitrile (PCN), markedly enhanced APAP-induced hepatic injury, as revealed by increased serum ALT levels and hepatic centrilobular necrosis, in wild-type but not in PXR-null mice. Further analysis showed that following PCN treatment, PXR-null mice had lower CYP3A11 expression, decreased NAPQI formation, and increased maintenance of hepatic glutathione content compared to wild-type mice. Thus, these results suggest that PXR plays a critical role in APAP-induced hepatic toxicity, probably by inducing CYP3A11 expression and hence increasing bioactivation.  
  Address Laboratory of Metabolism, CCR, NCI, NIH, Bethesda, Maryland 20892, USA  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1096-6080 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:15456926 Approved no  
  Call Number (up) refbase @ user @ Serial 71  
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Author Carroll, G.L.; Matthews, N.S.; Hartsfield, S.M.; Slater, M.R.; Champney, T.H.; Erickson, S.W. openurl 
  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  
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  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 (up) 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. openurl 
  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  
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  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 (up) refbase @ user @ Serial 97  
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Author Trim, C.M.; Moore, J.N.; Clark, E.S. openurl 
  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  
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  Notes PMID:9118094 Approved no  
  Call Number (up) refbase @ user @ Serial 99  
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