Inotropic mechanisms of dopexamine hydrochloride in horses.
Abstract: 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 micrograms/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 1, and beta 2-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. beta 1-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. beta 2-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, beta 1- and beta 2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.
Publication Date: 1992-08-01 PubMed ID: 1354950
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research article investigates the mechanisms behind the positive heart-strengthening effects of the drug dopexamine in horses. The study found that baroreflex activity and stimulation of beta 1 and beta 2-adrenergic receptors contribute significantly to these effects.
Introduction and Methodology
The researchers conducted the study on eight halothane-anesthetized horses. They specifically examined the cardiostimulatory effects of incrementally increased infusions of dopexamine, a drug known to strengthen the heart’s contractions.
- The effects of dopexamine were studied both before and after the administration of specific antagonists or drugs that counteract certain body actions.
- The antagonists were glycopyrrolate and chlorisondamine (to block muscarinic and nicotinic ganglionic activity respectively) and atenolol and ICI 118,551 (to block beta 1 and beta 2-adrenergic receptor activity respectively).
Results
The dopexamine infusions led to:
- A rise in heart rate, cardiac output (the quantity of blood the heart pumps per minute), systolic and mean arterial blood pressure, and maximum rate of left ventricular pressure development (a measure of heart contractility).
- A decrease in right atrial pressure and systemic vascular resistance (resistance to blood flow in blood vessels).
Impact of Antagonist Administration
The administration of glycopyrrolate, chlorisondamine, atenolol, and ICI 118,551 led to:
- Attenuation of the effects of dopexamine on cardiac output, blood pressures, and heart contractility.
- Potentiation (increase in potency) of dopexamine’s effect on heart rate.
- Decrease in heart rate, cardiac output, arterial blood pressure, and heart contractility from baseline values when beta 1-Adrenergic receptor was blocked.
- Further decrease in hemodynamic variables from baseline values and complete abolition of the cardiostimulatory effects of dopexamine when beta 2-Adrenergic receptor was blocked.
Conclusion
The study’s results indicate that baroreflex activity, and stimulation of beta 1- and beta 2-adrenergic receptors contribute to the positive heart-strengthening effects of dopexamine in horses. This could help better understand and optimize the use of dopexamine in veterinary medicine.
Cite This Article
APA
Muir WW.
(1992).
Inotropic mechanisms of dopexamine hydrochloride in horses.
Am J Vet Res, 53(8), 1343-1346.
Publication
Researcher Affiliations
- Department of Veterinary Clinical Sciences, Ohio State University, Columbus 43210.
MeSH Terms
- Adrenergic Agonists / pharmacology
- Adrenergic beta-Antagonists / pharmacology
- Animals
- Atenolol / pharmacology
- Blood Pressure / drug effects
- Cardiac Output / drug effects
- Dopamine / analogs & derivatives
- Dopamine / pharmacology
- Dopamine Antagonists
- Heart Rate / drug effects
- Hemodynamics / drug effects
- Horses / physiology
- Myocardial Contraction / drug effects
- Propanolamines / pharmacology
- Stimulation, Chemical
- Vascular Resistance / drug effects
Citations
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