Does exogenous thrombin alter vascular reactivity differently in ischemic compared to nonischemic canine coronary arteries?
Endothelial damage from ischemia shifts the coronary vascular response to thrombin from vasodilatation to vasoconstriction, suggesting a mechanism for coronary vasospasm.
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.
David D. Ku (Fri,) studied this question.