Inotropic mechanisms of dopexamine hydrochloride in horses

William W. Muir III From the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, OH 43210.

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 DVM, PhD

Summary

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 μg/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 β1, and β2-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/dtmax). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and + dP/dtmax responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. β1-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and + dP/dtmax from baseline values and markedly reduced the response to dopexamine infusion. β2-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on + dP/dtmax. These data indicate that baroreflex activity, β1- and β2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.

Summary

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 μg/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 β1, and β2-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/dtmax). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and + dP/dtmax responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. β1-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and + dP/dtmax from baseline values and markedly reduced the response to dopexamine infusion. β2-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on + dP/dtmax. These data indicate that baroreflex activity, β1- and β2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.

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