Major Contribution of Vasospasm-Induced Coronary Blood Flow Reduction to Anaphylactic Ventricular Dysfunction Assessed in Isolated Blood-Perfused Rat Heart

Abstract

(Cardiol J 2014; 21, 1: 11-17)

Blockade of β2-adrenoceptor, rather than β1-adrenoceptor, deteriorates cardiac anaphylaxis in isolated blood-perfused rat hearts

“…Experimental models of cardiac anaphylaxis were established in excised sensitized rat hearts perfused with crystalloids [7,8], in which coronary vasoconstriction and cardiac dysfunction, evidenced by a decrease in the maximum increasing rate of LV pressure (dP/dt max ), were induced by administration of the antigen ovalbumin into the coronary artery. Furthermore, new cardiac anaphylaxis models have recently been developed using the cross-circulated blood-perfusion method which permits analysis of LV mechanical works in excised whole heart preparations under more physiological conditions than crystalloid perfusion [9].…”

“…The purpose of this study was to determine the effects of b 1 -AR and b 2 -AR antagonists on coronary vasoconstriction and cardiac dysfunction during cardiac anaphylaxis in isolated blood-perfused rat hearts [9].…”

Kounis syndrome: A primary cause for the anaphylactic shock

“…In the important paper of Kuda et al [1] published in "Cardiology Journal" it was found that vasospasm-induced coronary flow reduction is a major contributory factor in anaphylactic ventricular dysfunction. The authors concluded that during anaphylaxis the ensuing left ventricular dysfunction is attributed mainly to coronary vasoconstriction-induced myocardial ischemia.…”

Authors’ response

“…We are grateful to Dr Kounis and Dr Soufras for their thoughtful insight into the mechanisms of anaphylactic shock and their evaluation of our article entitled "Major contribution of vasospasm--induced coronary blood flow reduction to anaphylactic ventricular dysfunction assessed in isolated blood-perfused rat heart" [1].…”

“…In our most recent study [1], we specifically addressed the question of whether the cardiac failure during anaphylaxis is primarily due to coronary vasoconstriction-induced myocardial ischemia or the direct negative inotropic effect of chemical mediators, using the method of the imposed constriction of coronary artery to reproduce the reduction in coronary blood flow during rat cardiac anaphylaxis. Consistent with the concept of 'Kounis syndrome', our study suggests that anaphylactic ventricular dysfunction is attributed mainly to vasoconstriction-induced coronary flow reduction and resultant myocardial ischemia.…”