Cardiovascular responses to exogenous platelet-activating factor (PAF) in anesthetized ponies, and the effects of a PAF antagonist, WEB 2086

D. V. Wilson From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824.

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S. W. Eberhart From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824.

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N. E. Robinson From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824.

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R. Rice From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824.

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P. R. Gray From the Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824.

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SUMMARY

The effects of exogenous platelet-activating factor (paf) were determined in anesthetized ponies. Administration of paf induced a decrease in cardiac index that resulted in systemic hypotension. This was followed by tachycardia, hypertension, and a return of cardiac index to baseline. Pulmonary aterial pressure increased markedly because of pulmonary vasoconstriction. Exogenous paf also caused leukopenia and thrombocytopenia. The specific PAP receptor antagonist (WEB 2086) blocked all paf-induced changes. Flunixin meglumine, a cyclooxygenase inhibitor, abolished the pulmonary hypertension and tachycardia, and attenuated the systemic hypotension but did not change the paf-induced peripheral cellular changes. The paf antagonist also inhibited platelet aggregation induced by paf in vitro. The paf-induced changes are similar to those reported after endotoxin exposure in horses.

SUMMARY

The effects of exogenous platelet-activating factor (paf) were determined in anesthetized ponies. Administration of paf induced a decrease in cardiac index that resulted in systemic hypotension. This was followed by tachycardia, hypertension, and a return of cardiac index to baseline. Pulmonary aterial pressure increased markedly because of pulmonary vasoconstriction. Exogenous paf also caused leukopenia and thrombocytopenia. The specific PAP receptor antagonist (WEB 2086) blocked all paf-induced changes. Flunixin meglumine, a cyclooxygenase inhibitor, abolished the pulmonary hypertension and tachycardia, and attenuated the systemic hypotension but did not change the paf-induced peripheral cellular changes. The paf antagonist also inhibited platelet aggregation induced by paf in vitro. The paf-induced changes are similar to those reported after endotoxin exposure in horses.

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