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过去工作表明5-羟色胺(5-HT)拮抗儿茶酚胺升高所致缩血管效应,对休克机体具有保护作用。内毒素休克狗死前全血5-HT、血浆NA明显升高,临床流脑休克患儿死前尿中5-HT极低,儿茶酚胺极高。据此,我们推测此时血小板释放5-HT障碍,使拮抗儿茶酚胺作用减弱,与休克晚期循环系统失代偿有关。本工作选250g左右雄性Wistar大鼠,按Wichterman等方法结扎盲肠,并用9号针头在结扎后盲肠上穿三个孔,使形成腹膜炎模型。对照大鼠行假手术。术后20～24小时,大部分大鼠发生弥漫性腹膜炎休克死亡。死前半小时左右,精神蒌糜、不活动、行走缓慢或不能站立。术后20～24小时,发现有以上表现大鼠立即麻醉下取心脏血,荧光法测血浆5-HT,放射酶法测血浆NA,并计数外周血小板,
Past work has shown that serotonin (5-HT) antagonizes the vasoconstrictive effect of elevated catecholamines and has a protective effect against shock. Endotoxin shock dogs pre-death whole blood 5-HT, plasma NA increased significantly, the clinical pre-death mellitus in children with very low urinary 5-HT, catecholamines. Accordingly, we hypothesized that 5-HT release of platelets at this time, so that the antagonistic effect of catecholamines weakened, and the late decompensation of the circulatory system. This work selected about 250g male Wistar rats, according to Wichterman and other methods of ligation of the cecum, and 9 needles in the cecum after the ligation of the three holes, the formation of peritonitis model. Control rats were sham operated. Postoperative 20 to 24 hours, most rats died of diffuse peritonitis shock. Half an hour before death, the spirit of Mi, inactive, slow or unable to stand. Twenty to twenty-four hours after operation, we found that the above performance of rats was taken immediately under anesthesia, 5-HT was measured by fluorescence spectrophotometry, plasma NA was measured by radioimmunoassay, and peripheral platelets were counted.