Do deficiencies of endothelial derived relaxing factor contribute to myocardial stunning?

Myocardial stunning is a phenomenon in which ventricular function is depressed by prior ischemia and remains suboptimal when blood flow is resumed. It is also characterized by coronary vascular endothelial dysfunction that is related to the duration of ischemia and can result in protein leakage, myocardial hemorrhage, or increased coronary vascular resistance. It is thought that local vascular tone is regulated by endothelium derived relaxing factor (EDRF), a compound commonly believed to be identical to nitric oxide (NO). EDRF increases the effects of other vasodilators through the formation of cyclic guanosine monophosphate (cGMP) by guanylate cyclase. Patients with various cardiovascular disorders have been found to have dysfunction in the EDRF system, and EDRF paradoxically produces vasoconstriction in atherosclerotic arteries. Similarly, EDRF stimulation of vasodilation due to acetylcholine, calcium ionophores, or platelets appears to be reduced in coronary arteries that have been damaged by ischemia and reperfusion. By increasing EDRF production or inhibiting its breakdown, EDRF precursors such as L-arginine, the superoxide radical scavenger superoxide dismutase, nitroglycerin, and nitroprusside all cause vasodilation by increasing NO levels in the setting of myocardial ischemia. These therapies may also improve local "microvascular" function, thereby improving ventricular function.