Hirooka Y, Egashira K, Imaizumi T, Tagawa T, Kai H, Sugimachi M, Takeshita A
Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
J Am Coll Cardiol. 1994 Oct;24(4):948-55. doi: 10.1016/0735-1097(94)90854-0.
The goal of this study was to determine whether the effect of L-arginine on endothelium-dependent vasodilation evoked with acetylcholine differs between the coronary and forearm vasculatures in humans.
Administration of L-arginine, a substrate in the production of endothelium-derived nitric oxide, may stimulate the release of nitric oxide.
Seven patients with normal coronary angiograms and seven with mild coronary artery disease and hypertension underwent coronary arteriography and an intracoronary Doppler catheter technique, and the diameter of the large epicardial coronary artery and coronary blood flow were measured. Forearm blood flow was measured by use of a strain gauge plethysmograph.
Before L-arginine administration, acetylcholine (1 to 30 micrograms/min) increased coronary blood flow with modest vasoconstriction of a large coronary artery. Acetylcholine (4 to 24 micrograms/min) also increased forearm blood flow. The acetylcholine-induced increases in coronary and forearm blood flow were significantly less in patients with coronary artery disease than in control patients. Intracoronary infusion of L-arginine at 50 mg/min did not alter responses of the large coronary artery diameter or coronary blood flow to acetylcholine in either group. In contrast, L-arginine at 10 mg/min significantly (p < 0.01) augmented the forearm blood flow response to acetylcholine (4 to 24 micrograms/min) to a similar extent in the two groups.
The effect of L-arginine on acetylcholine-induced vasodilation differs between the coronary and forearm vasculatures in humans. It is suggested that impaired acetylcholine-induced coronary and forearm vasodilation in patients with coronary artery disease and hypertension may not be related to a limited availability of L-arginine.
本研究的目的是确定在人类中，L-精氨酸对乙酰胆碱诱发的内皮依赖性血管舒张的影响在冠状动脉和前臂血管系统之间是否存在差异。
L-精氨酸是内皮源性一氧化氮产生过程中的一种底物，给予L-精氨酸可能会刺激一氧化氮的释放。
7例冠状动脉造影正常的患者和7例患有轻度冠状动脉疾病及高血压的患者接受了冠状动脉造影和冠状动脉内多普勒导管技术检查，并测量了大的心外膜冠状动脉直径和冠状动脉血流量。使用应变片体积描记器测量前臂血流量。
在给予L-精氨酸之前，乙酰胆碱（1至30微克/分钟）增加冠状动脉血流量，同时大冠状动脉出现适度血管收缩。乙酰胆碱（4至24微克/分钟）也增加前臂血流量。冠状动脉疾病患者中，乙酰胆碱诱导的冠状动脉和前臂血流量增加显著低于对照组患者。两组中，以50毫克/分钟的速度冠状动脉内输注L-精氨酸均未改变大冠状动脉直径或冠状动脉血流量对乙酰胆碱的反应。相比之下，10毫克/分钟的L-精氨酸使两组中前臂血流量对乙酰胆碱（4至24微克/分钟）的反应均显著增强（p<0.01），且增强程度相似。
在人类中，L-精氨酸对乙酰胆碱诱导的血管舒张的影响在冠状动脉和前臂血管系统之间存在差异。提示冠状动脉疾病和高血压患者中，乙酰胆碱诱导的冠状动脉和前臂血管舒张受损可能与L-精氨酸可用性受限无关。
