NITRIC-OXIDE REGULATES CORONARY BLOOD-FLOW AT VARIOUS CORONARY ARTERIAL PRESSURES IN INTACT PORCINE HEARTS

Nitric oxide (NO) is known to regulate basal coronary blood flow (CBF) . The objective of the present study was to examine the importance of NO in CBF regulation at various coronary arterial pressures (CAPs) in vivo. Experiments were performed in 11 open-chest pentobarbitone sodiu m anaesthetized pigs. CAP was reduced in steps by a hydraulic occluder on the mid left anterior descending coronary artery (LAD) before and after a 5-min intracoronary infusion of the inhibitor of NO synthesis, N-G-nitro-L-arginine (NOARG, 30 mu mol min(-1)). CAP was recorded and NOARG infused through a catheter inserted into the LAD just distal to the occluder. CBF was measured by Doppler flowmetry on the LAD. NOARG significantly reduced CBF by 11+/-4, 20+/-5, 10+/-3, 15+/-4, 19+/-2, 25+/-4 and 25+/-5 ml min(-1) 100 g(-1) (mean+/-SE) at CAPs of 30 (n = 6), 40 (n = 9), 50 (n = 9), 60 (n = 9), 70 (n = 9), 80 (n = 8) and 90 (n = 6) mmHg, respectively. These decrements were not statistically di fferent, but the percentage reductions in CBF after infusion of NOARG were significantly greatest at the lowest CAPs. The slight haemodynami c alterations induced by NOARG could not explain the reductions in CBF . Thus, the reductions in CBF after infusion of NOARG were caused by i nhibition of a continuous NO release from the coronary endothelium. Co ronary NO contributes significantly to CBF at all CAPs between 30 and 90 mmHg. The pronounced reduction in CBF during NO inhibition at the l ower CAPs indicates an important vasodilating role of intact endotheli um in a region supplied by a stenosed coronary artery.