Muramatsu K, Numaguchi K, Egashira K, Takahashi T, Kasuya H, Takeshita A
Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Coron Artery Dis. 1994 Oct;5(10):815-20.
To determine the role of an endothelium-derived relaxing factor (nitric oxide) in controlling basal coronary tone and coronary vasomotion after brief coronary occlusion (reactive hyperemia).
In 10 chronically instrumented conscious dogs, we studied the diameter changes of the large epicardial coronary artery and coronary blood flow in response to intracoronary administration of acetylcholine (0.1 and 1 microgram) and brief coronary occlusion for 5 and 20 s before and after intracoronary infusion of N-nitro-L-arginine (LNNA).
Intracoronary infusion of LNNA (1, 3, and 10 mg) decreased the diameter of the large epicardial coronary artery and coronary blood flow in a dose-dependent manner without altering arterial pressure and heart rate. LNNA (10 mg) significantly attenuated the increase in artery diameter and coronary blood flow by acetylcholine. The ratio of artery dilation to the blood flow response after acetylcholine was not affected by LNNA. LNNA (10 mg) significantly decreased the ratio of repayment to debt flow volume of reactive hyperemia, but did not affect the ratio of peak to resting flow; it also significantly attenuated the reactive dilation of the large epicardial coronary artery after reactive hyperemia. The ratio of artery dilation to repayment flow volume (micron/ml) during reactive hyperemia was attenuated significantly by LNNA.
These findings suggest that endothelium-derived nitric oxide may contribute to basal coronary tone and that reactive dilation of the large epicardial coronary artery during reactive hyperemia was caused by flow-mediated nitric oxide release, whereas coronary artery dilation after acetylcholine was caused largely by the direct receptor-mediated release of nitric oxide.
确定内皮源性舒张因子（一氧化氮）在短暂冠状动脉闭塞（反应性充血）后控制基础冠状动脉张力和冠状动脉血管运动中的作用。
在10只长期植入仪器的清醒犬中，我们研究了在冠状动脉内输注N-硝基-L-精氨酸（LNNA）前后，冠状动脉内给予乙酰胆碱（0.1和1微克）以及短暂冠状动脉闭塞5秒和20秒后，大的心外膜冠状动脉直径变化和冠状动脉血流情况。
冠状动脉内输注LNNA（1、3和10毫克）以剂量依赖方式降低了大的心外膜冠状动脉直径和冠状动脉血流，而未改变动脉血压和心率。LNNA（10毫克）显著减弱了乙酰胆碱引起的动脉直径和冠状动脉血流增加。乙酰胆碱后动脉扩张与血流反应的比值不受LNNA影响。LNNA（10毫克）显著降低了反应性充血的偿还与债务血流量比值，但不影响峰值与静息血流比值；它也显著减弱了反应性充血后大的心外膜冠状动脉的反应性扩张。反应性充血期间动脉扩张与偿还血流量（微米/毫升）的比值被LNNA显著减弱。
这些发现表明内皮源性一氧化氮可能有助于基础冠状动脉张力，并且反应性充血期间大的心外膜冠状动脉的反应性扩张是由血流介导的一氧化氮释放引起的，而乙酰胆碱后冠状动脉扩张主要是由直接受体介导的一氧化氮释放引起的。
