论文部分内容阅读
业已证实巴特尔综合征(Batter’s syndro-me)病人尿中PGE,及PGI_2主要代谢产物6—酮—PGF_(12)的量是增多的。PGE—M是肾外合成PGE的指数,它在巴氏症病人尿中往往是正常的。现已证明低钾血症者自身合成的PGS量是增多了。内分泌紊乱的一些疾病如高肾素血症、高醛固酮血症及对加压药耐受等都是继发于PGS尤其是PGI_2生产过剩之后。根据体内、体外实验证明PGI_2主要来源于血管及肺的内皮细胞,少部份来自肾间质细
It has been demonstrated in patients with Batter’s syndro-me urine PGE, and PGI 2 the main metabolite 6-keto-PGF 12 increased. PGE-M is an index of extra-renal synthesis of PGE, which is often normal in patients with PAS. It has been shown that hypokalemia patients own synthesis of PGS is increased. Some diseases of endocrine disorders such as high renin hyperlipidemia, hyperaldosteronism and tolerance to pressurized drugs are secondary to PGS, especially after PGI_2 overproduction. According to the in vitro and in vivo experiments, PGI 2 is mainly derived from endothelial cells of blood vessels and lungs,