Exaggerated atrial arachidonate metabolism in rabbit left ventricular myocardial infarction.

A S Evers; C G Dunkel; J E Saffitz; P Needleman

doi:10.1172/JCI112777

Exaggerated atrial arachidonate metabolism in rabbit left ventricular myocardial infarction.

A S Evers, C G Dunkel, J E Saffitz, and P Needleman

Published January 1, 1987 - More info

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Abstract

Isolated perfused rabbit hearts that have previously been subjected to in vivo left ventricular myocardial infarction respond to N-formylmethionyl-leucyl-phenylalanine (fMLP) or bradykinin (BK) administration with the synthesis of large quantities of eicosanoids. To anatomically localize these synthetic responses we studied the effects of fMLP and BK on eicosanoid synthesis in isolated atria and isolated perfused ventricles from normal and infarcted (4 d in vivo) rabbit hearts. These studies revealed that enhanced agonist-stimulated eicosanoid synthesis occurs largely in the right atria of infarcted hearts, a site distant from the zone of injury. Studies of exogenous arachidonate metabolism in microsomes prepared from various regions of the heart showed that while prostaglandin synthetic capacity is preferentially localized to the right atrium, right atria from normal and infarcted hearts have similar thromboxane and PGE2 synthetic capacity. These results demonstrate that enhanced agonist-stimulated eicosanoid synthesis following rabbit left ventricular myocardial infarction occurs largely in the right atrium, and that this effect is independent of the activity of prostaglandin synthetic enzymes.

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