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硝酸甘油和硝普钠是用于多种心血管疾病的强力血管扩张剂。硝酸甘油具有优先的扩张静脉作用,而硝普钠对静脉和动脉的扩张作用则均等。这些药物扩张人血管的真正机理尚不清。脐静脉内皮细胞培育显示,硝酸甘油能促进前列环素的合成,硝普钠则不能。本研究观察成人血管组织在硝酸甘油和硝普钠作用下产生前列环素的情况。方法:实验用血管是麻醉后立即取下的人大隐静脉,切成小环(0.5～1毫米厚)。将每一血管环(湿重30～35毫克)放入有含有1毫升无钙-镁缓冲液的聚丙烯小瓶中,用缓冲液轻洗几遍,然后放入1毫升含有钙和镁的 Hanks 缓冲盐溶液中(此缓冲液称为 HBSS)共15分钟,然后用硝酸甘油或硝普钠(5、10、100和1000微克/毫升的最后浓度),在37℃的缓冲液中培育15分钟,接着用(0.1毫克分子)花生四烯酸再处理15分钟.某些血管环在用硝酸甘油或硝普钠培育之前先用环氧化酶抑制剂——0.1毫克分子消炎痛处理15分钟,然后再加花生四烯酸培育,某些实验中对于用硝酸甘油或硝普钠加花生四烯酸培育之前的血管环,先用选择性血栓烷 A_2抑制
Nitroglycerin and sodium nitroprusside are potent vasodilators for many cardiovascular diseases. Nitroglycerin has a preferential dilatation of the vein, whereas sodium nitroprusside has equal effects on the dilatation of the veins and arteries. The exact mechanism by which these drugs expand human blood vessels is unclear. Umbilical vein endothelial cell culture shows that nitroglycerin can promote prostacyclin synthesis, sodium nitroprusside can not. This study observed adult vascular tissue in the role of nitroglycerin and sodium nitroprusside produce prostacyclin. Methods: The experimental blood vessels were removed from human saphenous vein immediately after anesthesia and cut into small rings (0.5-1 mm thick). Each vial ring (30-35 mg wet weight) was placed in a polypropylene vial containing 1 ml Ca-Mg-free buffer, washed several times with buffer, and then placed in 1 ml Hanks containing calcium and magnesium Buffered saline solution (this buffer is referred to as HBSS) for 15 minutes and then incubated with nitroglycerin or sodium nitroprusside (final concentrations of 5, 10, 100 and 1000 micrograms per milliliter) in a 37 ° C buffer for 15 minutes , Followed by 15 minutes with (0.1 mg) arachidonic acid Some vascular rings were treated with the cyclooxygenase inhibitor 0.1 mg of indomethacin for 15 minutes prior to incubation with nitroglycerin or sodium nitroprusside, Then add arachidonic acid culture, in some experiments for the use of nitroglycerin or nitroprusside plus arachidonic acid before culture of vascular rings, first with selective thromboxane A 2 inhibition