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1987年两组研究人员用化学和生物学分析方法分别发现血管内皮细胞释出一氧化氮(NO),其作用与被称为内皮舒张因子(EDRF)相同。现认为EDRF是内皮来源的NO。近五年的研究发现,NO在许多生理系统和病理生理状态中具有介质、信使或细胞功能调节因子的功能。NO是一种无色、微溶于水的气体,能被超氧化离子所破坏,可与氧化血红蛋白及其他含血红素的蛋白质结合,一旦与氧化血红蛋白结合,其生物作用迅速终止。在生物体内,NO的半衰期小于5秒钟。血管内皮细胞由精氨酸未端胍的氮原子合成NO。精氨酸的结构类似物能竞争性地抑制这种合成。NO的脂溶性很
In 1987, two groups of researchers, using chemical and biological assays, found that nitric oxide (NO) was released by vascular endothelial cells, respectively, in a manner similar to what is known as endothelium-dependent relaxation factor (EDRF). EDRF is now considered to be endothelial-derived NO. Nearly five years of research have found that NO has the function of mediators, messengers or cell function regulators in many physiological systems and pathophysiological states. NO is a colorless, slightly water-soluble gas that can be destroyed by superoxide ions and binds to oxyhemoglobin and other heme-containing proteins. Once combined with oxyhemoglobin, NO rapidly ends in its biological action. In vivo, the half-life of NO is less than 5 seconds. Vascular endothelial cells synthesize NO from the nitrogen atom of arginine no-terminal guanidine. Structural analogs of arginine competitively inhibit this synthesis. NO fat soluble