Kugiyama K, Motoyama T, Hirashima O, Ohgushi M, Soejima H, Misumi K, Kawano H, Miyao Y, Yoshimura M, Ogawa H, Matsumura T, Sugiyama S, Yasue H
Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.
J Am Coll Cardiol. 1998 Jul;32(1):103-9. doi: 10.1016/s0735-1097(98)00185-5.
This study sought to examine effect of vitamin C, an antioxidant, on the abnormal vasomotor reactivity in spasm coronary arteries.
Oxygen free radicals generated in the arterial walls have been shown to cause endothelial vasomotor dysfunction.
Responses of the epicardial arterial diameters of the left coronary arteries to the intracoronary infusion of acetylcholine (ACh) (10 and 50 microg/min) were measured by quantitative coronary angiography before and during combined intracoronary infusion of vitamin C (10 mg/min) or saline as a placebo in 32 patients with coronary spastic angina and in 34 control subjects.
Vitamin C infusion suppressed the constrictor response of the epicardial diameter to ACh in spasm coronary arteries but had no significant effect in the control coronary arteries (percent change in distal diameter in response to 10 microg/min of ACh [constriction (-), dilation (+), mean +/- SEM] before vitamin C: -8.2 +/- 2.9% in spasm arteries, +8.4 +/- 2.9%* in control arteries; during vitamin C: +0.2 +/- 3.8%* in spasm arteries, +7.2 +/- 1.3%* in control arteries [*p < 0.01 vs. spasm arteries before vitamin CI). The coronary sinus-arterial difference in plasma thiobarbituric acid reactive substances during ACh infusion, an indicator of lipid peroxidation in coronary circulation, was higher in patients with coronary spastic angina than in control subjects (p < 0.01) but was suppressed in patients with coronary spastic angina to comparable levels in control subjects by combined infusion of vitamin C. Saline infusion had no effect.
The results indicate that vitamin C attenuates vasomotor dysfunction in epicardial coronary arteries in patients with coronary spastic angina. Oxygen free radicals may at least in part play a role in the abnormal coronary vasomotor reactivity in response to ACh in spasm coronary arteries.
本研究旨在探讨抗氧化剂维生素C对痉挛冠状动脉异常血管舒缩反应性的影响。
已表明动脉壁中产生的氧自由基会导致内皮血管舒缩功能障碍。
通过定量冠状动脉造影术，在32例冠状动脉痉挛性心绞痛患者和34例对照受试者中，于冠状动脉内联合输注维生素C（10毫克/分钟）或生理盐水作为安慰剂之前及期间，测量左冠状动脉心外膜动脉直径对冠状动脉内输注乙酰胆碱（ACh）（10和50微克/分钟）的反应。
输注维生素C可抑制痉挛冠状动脉心外膜直径对ACh的收缩反应，但对对照冠状动脉无显著影响（维生素C输注前，对10微克/分钟ACh反应的远端直径变化百分比[收缩（-），舒张（+），平均值±标准误]：痉挛动脉中为-8.2±2.9%，对照动脉中为+8.4±2.9%；维生素C输注期间：痉挛动脉中为+0.2±3.8%，对照动脉中为+7.2±1.3%*[*与维生素C输注前的痉挛动脉相比，p<0.01]）。ACh输注期间血浆硫代巴比妥酸反应性物质的冠状窦-动脉差值（冠状动脉循环中脂质过氧化的指标），冠状动脉痉挛性心绞痛患者高于对照受试者（p<0.01），但通过联合输注维生素C，冠状动脉痉挛性心绞痛患者的该差值被抑制至与对照受试者相当的水平。输注生理盐水无作用。
结果表明，维生素C可减轻冠状动脉痉挛性心绞痛患者心外膜冠状动脉的血管舒缩功能障碍。氧自由基可能至少部分参与了痉挛冠状动脉对ACh异常的冠状动脉血管舒缩反应性。
