Coronary vascular reactivity after acute myocardial ischemia.
Exogenous thrombin produced a biphasic response (a potent dose-related vasodilatation followed by vasoconstriction) in nonischemic canine coronary arteries. The vasodilatation was not blocked by propranolol, atropine, or indomethacin, but was completely blocked by heparin or denudation of the intimal endothelial cells. A similar loss of vasodilating response to thrombin occurred in ischemic coronary arteries with a concomitant enhancement of vasoconstriction. This study indicates that altered responses to thrombin in coronary arteries with damaged endothelium may play an important role in the pathogenesis of coronary vasospasm.
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D004727:Endothelium / Q000187:drug effects; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000503:physiopathology*; D013917:Thrombin / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects; D014666:Vasomotor System / Q000187:drug effects; D014700:Verapamil / Q000494:pharmacology
D014700:Verapamil; D013917:Thrombin