REGULATION OF NATIVE COLLATERAL VESSEL DILATION AFTER CORONARY-OCCLUSION IN THE DOG

The purpose of this study was to examine mechanisms involved in the response of native collaterals to coronary occlusion. In anesthetized dogs native collaterals were identified as vessels coursing between the left anterior descending and left circumflex arteries using fluorescence angiography. After a left anterior descending occlusion in 12 dogs, collaterals <100 mu m in diameter progressively dilated by 21 +/- 4% (n = 12) 1 min after occlusion and by 39 +/- 6% 15 min after occlusion. Collaterals > 100 mu m in diameter did not dilate after coronary occlusion. N-G-nitro-L-arginine (1 mg/min intracoronary) caused constriction under basal conditions in collaterals < 100 mu m but did not prevent the dilation of collaterals after occlusion. In contrast, glibenclamide (10(-5) M), an inhibitor of ATP-sensitive potassium channels, had no effect on baseline diameter of collaterals < 100 mu m diameter but completely prevented dilation of collaterals after occlusion. We conclude that collaterals are not maximally dilated immediately after a coronary occlusion but rather progressively dilate for at least 15 min after an occlusion. This dilation of native collaterals after an occlusion is not mediated by release of an endothelium-derived relaxing factor derived from L-arginine but is mediated by activation of ATP-sensitive K+ channels.