BACKGROUND: The regulation of appetite and food intake in birds are implemented as complex homeostatic mechanisms at different levels of control. OBJECTIVES: The current research aimed to investigate the effects of glycine and strychnine-sensitive receptors on food intake induced with dopamine in neonatal broiler-type chickens. METHODS: This study was conducted in five experiments (each consisting of four treatment groups with 12 birds). In experiment 1, chickens in the control group received intracerebroventricular (ICV) injection of saline (with 0.1 % Evans Blue) and different doses of dopamine (10, 20, and 40 nmol) in treatments groups 2-4, respectively. Experiments 2 and 3 were designed similar to the experiment 1 except for the fact that chickens received different doses of glycine (50, 100, and 200 nmol) and strychnine (50, 100, and 200 nmol) instead of dopamine. Experiment 4 was performed to investigate the mediatory role of strychnine (100 nmol) on food intake induced with dopamine (40 nmol). Moreover, experiment 5 investigated the interaction between non-effective doses of glycine (50 nmol) and dopamine (10 nmol) and their interplay on food intake. Afterwards, cumulative food intake based on bodyweight percentage (BW %) was measured at 30, 60, and 120 minutes after the injection. RESULTS: The obtained findings revealed that effective doses of dopamine and glycine dose-dependently induced hypophagia in neonatal meat-type chickens (p < /em>≤0.05). In addition, injection of strychnine increased food intake and also inhibited the hypophagic effect induced by dopamine (p < /em>≤0.05). Furthermore, co-administration of non-effective doses of glycine and dopamine significantly decreased food intake compared to the groups which only received dopamine or glycine (p < /em>≤0.05). CONCLUSIONS: Our findings suggested that strychnine-sensitive receptors may have a mediatory role in food intake induced by dopamine. Additionally, it seems that glycine and dopamine probably have synergistic effects on food intake control in neonatal meat-type chickens.

We evaluated the effectiveness of 2 dopamine antagonists as treatments for fescue toxicosis in horses. Sixteen gravid mares were assigned by breed and expected foaling date to 1 of 3 treatment groups: endophyte-infested control 1.1 mg of domperidone/kg of body weight/d; and 3.3 mg of sulpiride/kg/d. Mares were pastured on endophyte-infected fescue and received 0.454 kg of a corn and dried molasses carrier containing the drug treatment. Treatment started 30 days prior to expected foaling date and continued until parturition. Blood samples were collected, and mammary gland scores were recorded every 5 days. Body weight and body condition scores were obtained every 28 days. Serum was analyzed for prolactin, progesterone, and estradiol-17beta concentrations. Domperidone-treated mares had shorter (P = 0.09) gestation duration and foaled closer (P = 0.07) to their expected parturition date than did control mares. Mammary gland scores were higher (P < 0.05) for domperidone-treated mares than for control mares. By 4 and 9 days after the start of treatment, serum prolactin concentration was higher P < 0.05) in domperidone-treated mares and sulpiride-treated mares, respectively, than in control mares. Domperidone- and and sulpiride-treated mares had higher (P < 0.05) serum progesterone and lower (P < 0.01) estradiol-17beta concentrations than did control mares. These results indicate that domperidone may offer considerable potential as a treatment for fescue toxicosis in horses.

Objective: To assess the effects of dopamine and dobutamine on the blood pressure of isoflurane-anesthetized Hispaniolan Amazon parrots (Amazona ventralis). Animals: 8 Hispaniolan Amazon parrots. Procedures: A randomized crossover study was conducted. Each bird was anesthetized (anesthesia maintained by administration of 2.5% isoflurane in oxygen) and received 3 doses of each drug during a treatment period of 20 min/dose. Treatments were constant rate infusions (CRIs) of dobutamine (5, 10, and 15 μg/kg/min) and dopamine (5, 7, and 10 μg/kg/min). Direct systolic, diastolic, and mean arterial pressure measurements, heart rate, esophageal temperature, and end-tidal partial pressure of CO2 were recorded throughout the treatment periods. Results: Mean ± SD of the systolic, mean, and diastolic arterial blood pressures at time 0 (initiation of a CRI) were 132.9 ± 22.1 mm Hg, 116.9 ± 20.5 mm Hg, and 101.9 ± 22.0 mm Hg, respectively. Dopamine resulted in significantly higher values than did dobutamine for the measured variables, except for end-tidal partial pressure of CO2. Post hoc multiple comparisons revealed that the changes in arterial blood pressure were significantly different 4 to 7 minutes after initiation of a CRI. Overall, dopamine at rates of 7 and 10 μg/kg/min and dobutamine at a rate of 15 μg/kg/min caused the greatest increases in arterial blood pressure. Conclusions and Clinical Relevance: Dobutamine CRI at 5, 10, and 15 μg/kg/min and dopamine CRI at 5, 7, and 10 μg/kg/min may be useful in correcting severe hypotension in Hispaniolan Amazon parrots caused by anesthesia maintained with 2.5% isoflurane.

Cultured rat pituitary cells were studied to: determine the effects of ergovaline and loline on in vitro prolactin release; delineate the agonistic activity of these alkaloids at the D2 dopamine receptor, using 2 selective D2 dopamine receptor antagonists; and compare the efficacy of 2 dopamine receptor antagonists in reversing effects of the treatments on in vitro prolactin secretion. Ergovaline reduced in vitro prolactin release by at least 40% (P < 0.05) at concentrations of 10(-4),10(-6), and 10(-8) M. However, loline reduced (P < 0.05) prolactin release only at the highest concentration, 10(-4) M. Two standard dopamine agonists, dopamine and alpha-ergocryptine, were used to verify that the inhibitory control mechanisms of in vitro prolactin release were intact. Both compounds reduced prolactin release by at least 40% for concentrations of 10(-4), 10(-6), or 10(-8) M. Selective D2 dopamine receptor antagonists 10(-6) M, domperidone and sulpiride, reversed (P < 0.05) the effect of loline on in vitro prolactin release. However, only domperidone (10(-6) M) was able to reverse (P < 0.05) the effect of ergovaline and only at the lowest ergovaline concentration (10(-8) M). Domperidone was more effective (P < 0.05) in reversing the prolactin-suppressing effect of alpha-ergocryptine than was sulpiride. The dose-response curve for domperidone (cubic fit, P < 0.0001) indicated a threshold concentration (10(-7)M) for reversal of alpha-ergocryptine's (10(-8)M) effect on prolactin release. However, at similar concentration of sulpiride (quadratic fit, P < 0.007), a threshold level was not obtained. These data indicate that ergovaline and loline mayact as D2 dopamine receptor agonists. Additionally, domperidone seems to be a more potent drug for reversal of the alkaloids hypoprolactinenic effect in vitro than does sulpiride.

Changes in lateral cecal arterial blood flow, mean internal carotid arterial pressure, and heart rate caused by nasogastric administration of fenoldopam (3, 6, and 9 mg/kg of body weight), a selective agonist of dopaminergic receptors, were recorded in 7 healthy horses. Cecal arterial blood flow was significantly increased within 30 minutes after administration of fenoldopam at all 3 dosages, with the peak increases from baseline (67.8 +/- 17.5 ml/min) being 125 +/- 28, 120 +/- 22, and 153 +/- 32 ml/min for 3, 6, and 9 mg/kg, respectively. Although carotid arterial pressure did not change significantly after administration of fenoldopam at the dosage of 3 mg/kg, administration of fenoldopam at the dosages of 6 and 9 mg/kg significantly reduced carotid arterial pressure from 113 +/- 10 to 88 +/- 3 and 81 +/- 5 mm of Hg, respectively. Intravenous infusion of metoclopramide, a dopaminergic receptor antagonist, at the rate of 0.125 mg/kg/h, blocked the effect of fenoldopam on cecal arterial blood flow and carotid arterial pressure. It was concluded that dopaminergic receptors mediate alterations in local blood flow and systemic pressure in horses.

Mechanisms responsible for the positive inotropic effects of dopexamine were investigated in 8 halothane-anesthetized horses. The hemodynamic effects of increasing infusions of dopexamine (5, 10, 15 microgram/kg of body weight/min) were determined before and after sequential administration of specific antagonists. Using glycopyrrolate and chlorisondamine, and atenolol and ICI 118,551, muscarinic and nicotinic ganglionic, and beta, and beta-adrenergic receptor blockade, respectively, was induced. Dopexamine infusions induced increase in heart rate, cardiac output, systolic and mean arterial blood pressure, and maximal rate of left ventricular pressure development (+dP/dt(max)). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and +dP/dt(max) responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. beta-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and +dP/dt(max) from baseline values and markedly reduced the response to dopexamine infusion. beta-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on +dP/dt(max) These data indicate that baroreflex activity, beta- and beta 2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.

Lateral cecal arterial blood flow, carotid arterial pressure, heart rate, and mechanical activity in the duodenum, right ventral colon, cecal body, and cecal apex were measured in 6 conscious healthy horses for 60 minutes during and for 120 minutes after IV infusion of 0.9% NaCl solution (control) or fenoldopam. There were no significant changes in these measurements during or after infusion of 0.9% NaCl (saline) solution. Fenoldopam, a selective dopamine- 1 receptor agonist, was administered in saline solution at dosages of 0.01, 0.05, and 0.1 ug/kg/min. Intravenous infusion of fenoldopam at 0.01 ug/kg/min significantly increased heart rate, but did not change average carotid arterial pressure or lateral cecal arterial blood flow. Intravenous infusion of fenoldopam at both 0.05 and 0.1 ug/kg/min significantly increased heart rate, significantly decreased average carotid arterial pressure, and significantly increased lateral cecal arterial blood flow. Intravenous infusion of fenoldopam at 0.01, 0.05 and 0.1 ug/kg/min did not significantly change the mechanical activity measured by the area under the strain gauge defection curve for the duodenum, right ventral colon, cecal body, or cecal apex. These results suggest that dopaminergic-1 receptors are present on the colonic vascudopaminergic-1 receptors exist on the visceral smooth muscle of the duodenum, right ventral colon, cecal body, or cecal apex of horses.

Objective: To determine cardiopulmonary effects of incremental doses of dopamine and phenylephrine during isoflurane-induced hypotension in cats with hypertrophic cardiomyopathy (HCM). Animals: 6 adult cats with severe naturally occurring HCM. Procedures: Each cat was anesthetized twice (once for dopamine treatment and once for phenylephrine treatment; treatment order was randomized). Hypotension was induced by increasing isoflurane concentration. Cardiopulmonary data, including measurement of plasma concentration of cardiac troponin I (cTnI), were obtained before anesthesia, 20 minutes after onset of hypotension, and 20 minutes after each incremental infusion of dopamine (2.5, 5, and 10 μg/kg/min) or phenylephrine (0.25, 0.5, and 1 μg/kg/min). Results: Mean ± SD end-tidal isoflurane concentration for dopamine and phenylephrine was 2.44 ± 0.05% and 2.48 ± 0.04%, respectively. Cardiac index and tissue oxygen delivery were significantly increased after administration of dopamine, compared with results after administration of phenylephrine. Systemic vascular resistance index was significantly increased after administration of phenylephrine, compared with results after administration of dopamine. Oxygen consumption remained unchanged for both treatments. Systemic and pulmonary arterial blood pressures were increased after administration of both dopamine and phenylephrine. Acid-base status and blood lactate concentration did not change and were not different between treatments. The cTnI concentration increased during anesthesia and infusion of dopamine and phenylephrine but did not differ significantly between treatments. Conclusions and Clinical Relevance: Dopamine and phenylephrine induced dose-dependent increases in systemic and pulmonary blood pressure, but only dopamine resulted in increased cardiac output. Hypotension and infusions of dopamine and phenylephrine caused significant increases in cTnI concentrations.

Objectives-To determine effects of commonly used diuretic treatments on glomerular filtration rate (GFR), renal blood flow (RBF), and urine output (UO) and compare 2 methods of GFR measurement in healthy awake cats. Animals-8 healthy cats. Procedure-In a randomized crossover design, cats were randomly allocated to 4 groups: control; IV administration of fluids; IV administration of fluids and mannitol; and IV administration of fluids, dopamine, and furosemide. Inulin and para-aminohippuric acid were used for determination of plasma clearance for GFR and RBF, respectively. Plasma clearance of technetium-Tc-99m-diethylenetriaminepentacetic acid (99mTc-DTPA) was also used for GFR determination. Results-Furosernide-dopamine induced the largest UO, compared with other groups. Both mannitol and fluid therapy increased RBF, compared with the control group. Mannitol, and not fluid therapy, increased RBF, compared with furosemide-dopamine. There were significant differences in GFR values calculated from 99mTc-DTPA and inulin clearances between the 2 groups. In all groups, use of 99mTc-DTPA caused underestimation of GFR, compared with use of inulin. Conclusions and Clinical Relevance-In healthy awake cats, administration of furosemide-dopamine did not increase GFR or RBF despite increased UO. Fluid therapy and fluid therapy plus mannitol improved RBF. Determination of GFR by use of 99mTc-DTPA cannot always be substituted for inulin clearance when accurate measurement is required.

Objective-To describe neuroendocrine responses that develop in dogs subjected to prolonged periods of ventricular pacing. Animals-14 adult male hound-type dogs. Procedure-Samples were obtained and neuroendocrine responses measured before (baseline) and after 3 periods of ventricular pacing. A pacemaker was used to induce heart rates of 180, 200, and 220 beats/min (BPM). Each heart rate was maintained for 3 weeks before increasing to the next rate. Atrial natriuretic peptide, antidiuretic hormone, aldosterone, norepinephrine, epinephrine, and dopamine concentrations and plasma renin activity were measured. Severity of left ventricular compromise was estimated. Results-Shortening fraction decreased significantly with increasing heart rates (mean +/- SE, 35.5 +/- 1.4, 25.0 +/- 1.4, 19.5 +/- 1.9, and 12.2 +/- 2.3 for baseline, 180 BPM, 200 BPM, and 220 BPM, respectively). Atrial natriuretic peptide concentrations increased significantly at 180 BPM (44.1 +/- 3.0 pg/mL) and 200 BPM (54.8 +/- 5.5 pg/mL), compared with baseline concentration (36.8 +/- 2.6 pg/mL). Dopamine concentration increased significantly at 200 BPM (70.4 +/- 10.4 pg/mL), compared with baseline concentration (44.2 +/- 7.3 pg/mL). Norepinephrine concentrations increased significantly from baseline concentration (451 +/- 46.2 pg/mL) to 678 +/- 69.8, 856 +/- 99.6, and 1,003 +/- 267.6 pg/mL at 180, 200, and 220 BPM, respectively. Conclusions and Clinical Relevance-Dogs subjected to ventricular pacing for 9 weeks developed neuroendocrine responses similar to those that develop in humans with more chronic heart failure and, except for epinephrine concentrations, similar to those for dogs subjected to ventricular pacing for < 6 weeks.