Decreased flow reserve in "stunned" myocardium after a 10-min coronary occlusion.
The effect of brief reversible ischemia on coronary vascular function remains controversial. Studies using a 15-min coronary occlusion have reported an impairment of vasodilator reserve, whereas studies using shorter occlusions have not. To elucidate the relation between postischemic vascular abnormalities and duration of ischemic insult, we evaluated coronary reserve after a 10-min coronary occlusion in the same model previously used for a 15-min occlusion. Open-chest dogs (n = 12) underwent a 10-min left anterior descending coronary artery occlusion followed by reflow. Four hours after reperfusion, coronary resistance was higher in the postischemic "stunned" myocardium than in the nonischemic myocardium, both at rest and during adenosine-induced maximal vasodilation; in addition, all indexes of reactive hyperemia after a 40-s coronary occlusion were significantly lower than at baseline. There was no appreciable correlation between systolic wall thickening in the stunned myocardium and 1) the resting myocardial perfusion, 2) the hyperemia attained during adenosine, and 3) the hyperemic response to a 40-s coronary occlusion. The loss of coronary reserve was less than that previously observed after a 15-min occlusion, suggesting that the magnitude of the postischemic vascular abnormalities increases with the duration of the ischemic insult. In control dogs (n = 8), there was no change in coronary reserve. We conclude that a brief ischemic insult lasting only 10 min is sufficient to cause a prolonged increase in resting vascular resistance and a prolonged impairment in vasodilator responsiveness, both of which persist for at least 4 h, indicating the presence of a postischemic microvascular dysfunction. The severity of these vascular derangements is not related to the severity of the contractile depression, suggesting that they may represent a relatively independent phenomenon. The differences among previous studies may be due, in part, to the fact that the abnormalities observed after a 10-min occlusion are relatively subtle.
Triana
J F
JF
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.
Bolli
R
R
D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D003326:Coronary Circulation / Q000502:physiology*; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D004285:Dogs; D005260:Female; D006339:Heart Rate; D006439:Hemodynamics; D006940:Hyperemia / Q000503:physiopathology; D008297:Male; D015425:Myocardial Reperfusion; D012016:Reference Values; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D000241:Adenosine