Effects of prostacyclin (PGI2) on vulnerability to ventricular fibrillation in the normal and ischemic canine heart.
Prostacyclin (PGI2) has been shown to have a number of beneficial effects on the cardiovascular system. However, its effects on ventricular electrical properties remain unexplored. We studied the effects of this naturally occurring humoral agent on ventricular vulnerability in the normal heart and in two models of myocardial ischemia: coronary artery occlusion and release and ergonovine-induced coronary vasoconstriction. Prostacyclin lowered the vulnerable period threshold in the normal animal. PGI2 had no effect on ventricular vulnerability when the blood pressure was controlled with phenylephrine and was not protective during either occlusion or release. However, when blood pressure was controlled, PGI2 did not reverse the vasoconstrictor and profibrillatory effects of ergonovine.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology*; D004874:Ergonovine / Q000494:pharmacology; D005260:Female; D006321:Heart / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D011453:Prostaglandins / Q000494:pharmacology*; D014693:Ventricular Fibrillation / Q000517:prevention & control*
D011453:Prostaglandins; D011464:Epoprostenol; D004874:Ergonovine