人冠状动脉血管内皮依赖性舒张功能：一氧化氮合成抑制的影响

Flow-mediated vasodilation of human epicardial coronary arteries: effect of inhibition of nitric oxide synthesis.

作者信息

Shiode N, Morishima N, Nakayama K, Yamagata T, Matsuura H, Kajiyama G

机构信息

Department of Internal Medicine, Hiroshima University School of Medicine, Japan.

出版信息

J Am Coll Cardiol. 1996 Feb;27(2):304-10. doi: 10.1016/0735-1097(95)00465-3.

DOI:10.1016/0735-1097(95)00465-3

PMID:8557898

Abstract

OBJECTIVES

This study sought to investigate the role of nitric oxide, an endothelium-derived relaxing factor, in flow-mediated vasodilation in human epicardial coronary arteries.

BACKGROUND

Endothelium-derived relaxing factors may be released from the coronary artery endothelium in response to increases in blood flow.

METHODS

We studied the effect of the nitric oxide synthesis inhibitor NG-monomethyl-L-arginine (L-NMMA) on the flow-mediated vasodilation of epicardial coronary arteries in 12 patients, using quantitative angiographic and Doppler flow velocity measurements. Adenosine at 100 micrograms/min was infused into the left anterior descending coronary artery to test the dilator response of the proximal artery to increases in blood flow. Acetylcholine at 3 and 30 micrograms/min was infused into the left coronary ostium to determine endothelium-dependent vasodilation of the proximal left anterior descending artery. Adenosine and acetylcholine were infused before and after the intracoronary infusion of L-NMMA (25 mumol/min for 5 min).

RESULTS

Infusion of L-NMMA caused a significant decrease in the baseline diameter of the proximal left anterior descending artery (from 2.90 +/- 0.14 to 2.74 +/- 0.13 mm [mean +/- SEM], p < 0.01). Adenosine increased coronary blood flow before and after L-NMMA (+399.5 +/- 27.5% and +511.9 +/- 33.3%, respectively). Flow-mediated vasodilation was observed in the proximal left anterior descending artery before and after L-NMMA (+9.2 +/- 1.5%, p < 0.01 and +8.6 +/- 2.1%, p < 0.01, respectively). A dose of 3 micrograms/min of acetylcholine significantly dilated the proximal left anterior descending artery before L-NMMA (+7.6 +/- 1.0%, p < 0.01), but acetylcholine-induced vasodilation was attenuated after L-NMMA (-1.8 +/- 1.0%).

CONCLUSIONS

Our data suggest that nitric oxide modulates basal coronary artery tone but that mediators other than nitric oxide may be responsible for the flow-mediated vasodilation of human epicardial coronary arteries.

摘要

目的

本研究旨在探讨内皮源性舒张因子一氧化氮在人类心外膜冠状动脉血流介导的血管舒张中的作用。

背景

内皮源性舒张因子可能会因血流增加而从冠状动脉内皮释放。

方法

我们使用定量血管造影和多普勒流速测量，研究了一氧化氮合成抑制剂NG-单甲基-L-精氨酸（L-NMMA）对12例患者心外膜冠状动脉血流介导的血管舒张的影响。以100微克/分钟的速度向左前降支冠状动脉注入腺苷，以测试近端动脉对血流增加的扩张反应。以3微克/分钟和30微克/分钟的速度向左冠状动脉口注入乙酰胆碱，以确定左前降支近端动脉的内皮依赖性血管舒张。在冠状动脉内注入L-NMMA（25微摩尔/分钟，持续5分钟）之前和之后注入腺苷和乙酰胆碱。

结果

注入L-NMMA导致左前降支近端动脉的基线直径显著减小（从2.90±0.14毫米降至2.74±0.13毫米[平均值±标准误]，p<0.01）。在L-NMMA注射前后，腺苷均增加了冠状动脉血流量（分别为+399.5±27.5%和+511.9±33.3%）。在L-NMMA注射前后，左前降支近端动脉均观察到血流介导的血管舒张（分别为+9.2±1.5%，p<0.01和+8.6±2.1%，p<0.01）。在L-NMMA注射前，3微克/分钟剂量的乙酰胆碱使左前降支近端动脉显著扩张（+7.6±1.0%，p<0.01），但在L-NMMA注射后，乙酰胆碱诱导的血管舒张减弱（-1.8±1.0%）。