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

The purpose of this study was to examine mechanisms involved in the re sponse of native collaterals to coronary occlusion. In anesthetized do gs native collaterals were identified as vessels coursing between the left anterior descending and left circumflex arteries using fluorescen ce 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 occ lusion. N-G-nitro-L-arginine (1 mg/min intracoronary) caused constrict ion under basal conditions in collaterals < 100 mu m but did not preve nt the dilation of collaterals after occlusion. In contrast, glibencla mide (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 conc lude that collaterals are not maximally dilated immediately after a co ronary occlusion but rather progressively dilate for at least 15 min a fter an occlusion. This dilation of native collaterals after an occlus ion is not mediated by release of an endothelium-derived relaxing fact or derived from L-arginine but is mediated by activation of ATP-sensit ive K+ channels.