一氧化氮(NO)是由NO合成酶产生的松弛平滑肌的一种内源性介质。NO合成酶将L-精氨酸转变成L-瓜氨酸及NO。在平滑肌,NO合成酶可被内毒素及其他细菌产物诱导。由于结肠腔含有大量细菌产物,作者假设结肠壁NO:精氨酸途径的病理性激活能触发中毒性巨结肠。为此研究了4例因中毒性巨结肠(平片下直径>6.5cm并有系统性中毒)作结肠切除的溃结病人及因癌症作结肠切除的对照病人的结肠标本。对照组无一例有肠麻痹;标本取自肿瘤远侧,肉眼观正常。通过孵育产生的~(14)C-L-瓜氨酸测定肌肉标本新鲜匀浆中NO合成酶活力。通过加入EGTA来识别Ca~(2+)依赖或非Ca~(2+)依赖同工酶。对照标本的肌条在加或不加内毒素的器官浴培育6h,然后作NO合成酶测定。 结果:中毒性巨结肠标本的肌层中Ca~(2+)依赖活性高于对照组(2.0±0.4pmol/min·mg蛋白质比0.6±0.6,P<0.05)。同样,非Ca~(2+)依赖活性在巨结肠病例中较对照组高(1.7±0.5比0.5±0.2,P<0.05)。对照 Nitric oxide (NO) is an endogenous mediator of relaxation of smooth muscle produced by NO synthase. NO synthase converts L-arginine to L-citrulline and NO. In the smooth muscle, NO synthase can be induced by endotoxin and other bacterial products. Since the colon lumen contains a large number of bacterial products, the authors hypothesized that the pathological activation of the NO: arginine pathway in the colon wall could trigger toxic megacolon. For this purpose, four colon specimens of patients with ulcerative colitis undergoing colonic resection due to toxic megacolon (flat-bottom diameter> 6.5 cm and systemic poisoning) and colonic resection for cancer were studied. No case of control group had intestinal paralysis; specimens taken from the distal tumor, the naked eye was normal. The activity of NO synthase in fresh homogenate of muscle samples was determined by incubation of ~ (14) C-L-citrulline. Ca 2+ -dependent or non-Ca 2+ -dependent isoenzymes were identified by adding EGTA. The muscle strips of the control specimens were incubated for 6 h in organ baths with or without endotoxin and then assayed for NO synthase. Results: Ca 2+ - dependent activity in the muscle of toxic giant colon specimens was higher than that in the control group (2.0 ± 0.4 pmol / min · mg · h -1 protein: 0.6 ± 0.6, P <0.05). Similarly, non-Ca2 + -dependent activity was (1.7 ± 0.5 vs. 0.5 ± 0.2, P <0.05) higher in the case of megacolon as compared with the control. Control