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硝酸盐引起的冠状动脉扩张并非由前列腺素系统介导:一项定量电影血管造影研究。

Coronary vasodilation by nitrates is not mediated by the prostaglandin system: a quantitative cineangiographic study.

作者信息

Simonetti I, De Caterina R, Michelassi C, Marzilli M, de Nes M, L'Abbate A

出版信息

J Am Coll Cardiol. 1986 Dec;8(6):1263-70. doi: 10.1016/s0735-1097(86)80295-9.

DOI:10.1016/s0735-1097(86)80295-9
PMID:3782633
Abstract

The possible role of prostaglandins in mediating large coronary artery vasodilation by nitrates was investigated by quantitative magnification coronary angiography. The effects of aspirin (1 g systemically and 100 mg intracoronary) in preventing large coronary artery vasodilation induced by intracoronary isosorbide dinitrate was investigated in 16 patients. Of these, 5 received 0.3 mg (Group 1A) and 11 received 3 mg (Group 1B) intracoronary isosorbide dinitrate, before and 15 minutes after aspirin. Relative to control, 0.3 mg isosorbide dinitrate induced a 19 +/- 9% (mean +/- SD) (p less than 0.01) and 19.5 +/- 11% (p less than 0.01) increase in coronary diameter before and after aspirin, respectively (p = NS). Changes after 3 mg isosorbide were 23 +/- 12% (p less than 0.01) and 26.5 +/- 14% (p less than 0.01), respectively, before and after aspirin (p = NS). In 10 additional patients (Group 2), the effect of the same dose of aspirin on rest coronary artery tone was assessed: changes relative to control were 0.9 +/- 5.5% (p = NS) minutes after aspirin. The intracoronary administration of 3 mg isosorbide dinitrate produced a 24.7 +/- 11% increase in coronary diameter (p = NS versus pre- and postaspirin isosorbide in Group 1B). Urinary 6-ketoprostaglandin-F1 alpha values in urine samples collected in the 8 hours before and the 8 hours after the study in five patients in Group 1B and five patients of Group 2, revealed a 36 +/- 14% (mean +/- SD) reduction in excretion of prostacyclin (p less than 0.01). These data rule out a role for prostaglandins both in mediating dilation of large coronary arteries by nitrates and in affecting their vascular tone at rest.

摘要

通过定量放大冠状动脉造影术研究了前列腺素在硝酸盐介导的大冠状动脉血管舒张中的可能作用。在16例患者中研究了阿司匹林(全身1g和冠状动脉内100mg)预防冠状动脉内硝酸异山梨酯诱导的大冠状动脉血管舒张的效果。其中,5例接受0.3mg(1A组),11例接受3mg(1B组)冠状动脉内硝酸异山梨酯,分别在服用阿司匹林前和服用后15分钟。相对于对照,0.3mg硝酸异山梨酯在服用阿司匹林前后分别使冠状动脉直径增加19±9%(平均值±标准差)(p<0.01)和19.5±11%(p<0.01)(p=无显著性差异)。3mg硝酸异山梨酯服用前后的变化分别为23±12%(p<0.01)和26.5±14%(p<0.01),在服用阿司匹林前后(p=无显著性差异)。在另外10例患者(2组)中,评估了相同剂量阿司匹林对静息冠状动脉张力的影响:相对于对照,服用阿司匹林后几分钟的变化为0.9±5.5%(p=无显著性差异)。冠状动脉内给予3mg硝酸异山梨酯使冠状动脉直径增加24.7±11%(与1B组服用阿司匹林前后的硝酸异山梨酯相比,p=无显著性差异)。在1B组的5例患者和2组的5例患者中,研究前8小时和研究后8小时收集的尿液样本中的尿6-酮前列腺素-F1α值显示,前列环素排泄减少36±14%(平均值±标准差)(p<0.01)。这些数据排除了前列腺素在硝酸盐介导的大冠状动脉扩张以及影响其静息血管张力方面的作用。

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