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Journal of Pharmacology And Experimental Therapeutics, Vol. 182, Issue 2, 227-238, 1972
Copyright © 1972 by American Society for Pharmacology and Experimental Therapeutics


EFFECTS OF EXOGENOUS AND IMMUNOLOGICALLY RELEASED HISTAMINE ON THE ISOLATED HEART: A QUANTITATIVE COMPARISON

ROBERTO LEVI 1

1 Department of Pharmacology, Cornell University Medical College, New York, New York

Histamine, present in the heart of various mammals including man, may be mobilized during immediate hypersensitivity reactions. With the purpose of ascertaining the role of histamine in immediate hypersensitivity reactions of the heart, the relationship between cardiac anaphylaxis and effects of histamine was explored. Isolated coronary-perfused guinea pig hearts were used; histamine was administered intra-aortically or released in a graded fashion by passive anaphylaxis. Both exogenous and endogenous histamine induced positive inotropic and chronotropic effects and prolonged atrioventricular conduction. All of these effects were concentration-dependent, with the exception of the inotropic effect of endogenous histamine. Exogenous histamine increased the rate of coronary flow in a dose-dependent fashion, but at high concentrations atrioventricular block developed and the increments in flow rate became progressively smaller. During anaphylaxis, conduction arrhythmias appeared more frequently and were more severe than with exogenous histamine; this coincided with a decrease in coronary flow rate. The comparison between the effects of exogenous and endogenous histamine indicated the same mechanism of action for both. The greater quantitative effect of endogenous histamine reflected its larger concentration at the effector sites. The results suggest that in the anaphylaxis of the isolated guinea-pig heart, tachycardia and delay in atrioventricular conduction are of histaminergic origin and that the fall in coronary flow rate is the consequence of conduction arrhythmia.

Submitted on December 16, 1971
Accepted on April 21, 1972




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Copyright © 1972 by the American Society for Pharmacology and Experimental Therapeutics.