BACKGROUND: Brief ischemic episodes that induce stunning of the myocardium may also induce stunning of the coronary endothelium. To test this hypothesis, we examined both in vivo and in vitro responses of canine coronary arteries exposed to brief ischemia. METHODS AND RESULTS: Functional recovery of the endothelium was examined in vivo during reperfusion after 15 minutes of ischemia. Vasodilatory responses to acetylcholine were severely impaired during the first hour of reperfusion but gradually improved over a 90-minute period after ischemia. The vasoconstrictive response to U46619 was enhanced for the first 30 minutes of reperfusion and returned to normal within 60 minutes. In vitro vasomotor responses to potassium chloride, acetylcholine, bradykinin, and sodium nitroprusside were examined in isolated segments of canine coronary arteries preexposed in vivo to brief ischemia (10-30 minutes) and 20 minutes of reperfusion. The results showed enhanced contractile responses and blunted endothelium-dependent but not endothelium-independent vasodilatory responses of arterial rings subjected to 10 minutes of ischemia. Twenty and 30 minutes of ischemia completely impaired endothelium-dependent vasodilation. When reperfusion was extended to 120 minutes after 15 minutes of ischemia, vasodilatory responses to acetylcholine had recovered by almost 90%. Examination of endothelial integrity by transmission electron microscopy after 10-15 minutes of ischemia revealed no evidence of structural damage. Twenty and 30 minutes of ischemia induced cytoplasmic vacuolation, partial detachment of endothelium, and swelling of cytoplasmic organelles. CONCLUSIONS: These data support the hypothesis that brief ischemia-reperfusion induces stunning of endothelium in which endothelium-dependent vasodilatory function is impaired temporarily without morphological damage.
BACKGROUND: Brief ischemic episodes that induce stunning of the myocardium may also induce stunning of the coronary endothelium. To test this hypothesis, we examined both in vivo and in vitro responses of canine coronary arteries exposed to brief ischemia. METHODS AND RESULTS: Functional recovery of the endothelium was examined in vivo during reperfusion after 15 minutes of ischemia. Vasodilatory responses to acetylcholine were severely impaired during the first hour of reperfusion but gradually improved over a 90-minute period after ischemia. The vasoconstrictive response to U46619 was enhanced for the first 30 minutes of reperfusion and returned to normal within 60 minutes. In vitro vasomotor responses to potassium chloride, acetylcholine, bradykinin, and sodium nitroprusside were examined in isolated segments of canine coronary arteries preexposed in vivo to brief ischemia (10-30 minutes) and 20 minutes of reperfusion. The results showed enhanced contractile responses and blunted endothelium-dependent but not endothelium-independent vasodilatory responses of arterial rings subjected to 10 minutes of ischemia. Twenty and 30 minutes of ischemia completely impaired endothelium-dependent vasodilation. When reperfusion was extended to 120 minutes after 15 minutes of ischemia, vasodilatory responses to acetylcholine had recovered by almost 90%. Examination of endothelial integrity by transmission electron microscopy after 10-15 minutes of ischemia revealed no evidence of structural damage. Twenty and 30 minutes of ischemia induced cytoplasmic vacuolation, partial detachment of endothelium, and swelling of cytoplasmic organelles. CONCLUSIONS: These data support the hypothesis that brief ischemia-reperfusion induces stunning of endothelium in which endothelium-dependent vasodilatory function is impaired temporarily without morphological damage.