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EFFECTS OF ENDOTHELIUM-DERIVED RELAXANT FACTOR ON CORONARY RESISTANCE VESSELS

EFFECTS OF ENDOTHELIUM-DERIVED RELAXANT FACTOR ON CORONARY RESISTANCE VESSELS
内皮源性舒张因子对冠状动脉阻力血管的影响
批准号:
3899266
负责人:
A A QUYYUMI
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
我们之前已经证明了前臂的血管构筑 高血压患者对输液的反应较差 乙酰胆碱(Ach)能使内皮释放内皮-- 衍生松弛因子(EDRF)。在这项研究中,我们调查了 乙酰胆碱对冠脉内皮细胞膜电导和阻力的影响 不同胸痛证候患者的血管分布。 冠脉内注射乙酰胆碱对心外膜冠状动脉内径、血流量和冠脉流量的影响 16例心外膜冠状动脉正常和冠状动脉狭窄患者的冠脉阻力 胸痛,以及心外膜冠状动脉正常和 对肥厚型心肌病进行了研究。心外膜冠状动脉 直径无明显变化。然而,GCV流量增加了, 冠脉阻力随Ach的升高而逐渐降低。在10-8摩尔 Ach、GCV用量增加12+3%,10-7摩尔时,GCV流量增加 增加34±6%,10-6摩尔剂量时增加49±9%。与基线相比。 这提示血管内皮依赖性的冠状动脉阻力扩张。 血管的发生独立于心外膜冠状动脉的改变。因此,它 可想而知,内皮细胞可能调节冠状动脉阻力和 人流涌动。目前尚不能确定是否存在异常 阻力血管的血管扩张可能继发于内皮细胞 功能障碍,从而在某些情况下导致心肌缺血综合征 PTS。
英文摘要
We have previously demonstrated that the forearm vasculature of hypertensive patients is less responsive to the effects of infused acetylcholine (Ach) which causes the endothelium to release endothelium-- derived-relaxant factor (EDRF). In this study, we investigated the effect of Ach on the endothelium lining of coronary conductance and resistance vessels in patients with various chest pain syndromes. The effects of intracoronary Ach on epicardial coronary diameter, flow and coronary resistance in 16 pts with normal epicardial coronary arteries and chest pain, and those with normal epicardial coronary arteries and hypertrophic cardiomyopathy were studied. Epicardial coronary artery diameter did not change significantly. However, GCV flow increased and coronary vascular resistance decreased incrementally to Ach. At 10-8 molar dose of Ach, GCV flog increased by 12+3%; at 10-7 molar, GCV flow increased by 34+6%; at 10-6 molar dose, it increased by 49+9%. compared to baseline. This suggests that endothelium-dependent dilation of coronary resistance vessels occurs independent of epicardial coronary artery changes. Thus, it is conceivable that the endothelium may regulate coronary resistance and flow in man. It remains to be determined whether abnormalities of vasodilatation of resistance vessels my be secondary to endothelial dysfunction, and thus contribute to myocardial ischemic syndromes in some pts.
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