CHOLINERGIC AND ALPHA-ADRENERGIC CORONARY CONSTRICTION WITH INCREASING ISCHEMIA-REPERFUSION INJURY

Ischemia-reperfusion-induced injury of the coronary vasculature could result in an attenuated vasodilator or increased vasoconstrictor tone that might impact on myocardial recovery and viability. In 30 open-che st dogs the left circumflex coronary artery was occluded for 15 or 60 min and then reperfused, and responses to intracoronary acetylcholine, the alpha(1)-adrenergic agonist methoxamine, and the alpha(2)-adrener gic agonist BHT-933 (n = 10 each) were measured. In the experiments wi th 60 min of occlusion, triphenyltetrazolium chloride (TTC) staining w as used to distinguish reversibly (TTC+) and irreversibly (TTC-) injur ed myocardium. After 15 min of occlusion, the vasodilator response to acetylcholine was not altered but was significantly reduced in TTC+ su bendocardium and midmyocardium after 60 min of occlusion and was furth er reduced in TTC-subendocardium, midmyocardium, and also in subepicar dium. The vasoconstrictor responses to methoxamine and BHT-933 were no t altered after 15 or 60 min of occlusion in both TTC+ and TTC- myocar dium. Posterior wall thickening was not affected by acetylcholine, met hoxamine, or BHT-933. Thus, in reversibly injured myocardium after 15 min of occlusion, cholinergic and alpha-adrenergic coronary vasomotor responses are unchanged. With increasing duration of ischemia, reversi bly and even more so irreversibly injured reperfused myocardium are ch aracterized by an impaired cholinergic coronary vasodilation but not a n enhanced alpha-adrenergic coronary vasoconstriction.