硫喷妥钠昏迷诱导大鼠暴发性高氨血症

Fulminant hyperammonaemia induced by thiopental coma in rats.

作者信息

Ivnitsky Jury Ju, Rejniuk Vladimir L, Schäfer Timur V, Malakhovsky Vladimir N

机构信息

Military Toxicology and Medical Protection, Military Medical Academy, ul. Lebedeva 6, 194044 St. Petersburg, Russia.

出版信息

Toxicology. 2006 Jul 25;224(3):184-90. doi: 10.1016/j.tox.2006.04.002. Epub 2006 Apr 18.

DOI:10.1016/j.tox.2006.04.002

PMID:16704891

Abstract

Fulminant hyperammonaemia as a threshold effect of coma-inducing dose of sodium thiopental has been revealed in rats. Blood ammonia content increased progressively after the introduction of 1.0 LD(50) (but not 0.8 LD(50)) of sodium thiopental three times in 3h and five times in 18h. The urinary ammonia excretion was not impaired while the volatilization of ammoniac from the body of ST-treated rats was higher, giving evidence of the augmentation of ammonia production. Blood urea increased by one third despite of insignificant alterations of haematocrit and blood creatinine. Ammonia hyperproduction in the digestive tract could result from gastrointestinal stasis, which has been verified by roentgenography and confirmed by correlation of hyperammonaemia with the stool retardation. In thiopental coma rats the slope of a dose-dependent increase of the blood ammonia and the blood urea after the intraperitoneal injection of ammonium acetate did not exceed that in intact animals. So the ammonia hyperproduction in the digestive tract could be the main contributing cause of fulminant hyperammonaemia in rats with thiopental coma and thus be involved into pathogenesis of the coma.

摘要

在大鼠中已发现，硫喷妥钠诱导昏迷剂量引发的暴发性高氨血症呈阈值效应。在3小时内三次注射1.0 LD(50)（而非0.8 LD(50)）硫喷妥钠以及在18小时内五次注射后，血氨含量逐渐升高。硫喷妥钠处理的大鼠体内氨的挥发增加，尿氨排泄未受损害，这表明氨生成增加。尽管血细胞比容和血肌酐变化不显著，但血尿素增加了三分之一。消化道氨生成过多可能源于胃肠淤滞，这已通过X射线造影证实，且高氨血症与粪便排出延迟的相关性也证实了这一点。在硫喷妥钠昏迷大鼠中，腹腔注射醋酸铵后血氨和血尿素剂量依赖性增加的斜率不超过正常动物。因此，消化道氨生成过多可能是硫喷妥钠昏迷大鼠暴发性高氨血症的主要促成原因，进而参与昏迷的发病机制。