Hyperammoniemia in rats with barbiturate coma

Abstract

Sodium thiopental in the comatogenic (but not soporogenic) dose caused hyperammoniemia in rats. Blood ammonium level increased 3-fold within 3 h and 5-fold within 18 h. Blood urea level increased by one-third within 18 h against the background of unchanged creatinine level and hematocrit. Urinary excretion of ammonium did not decrease, while its release with exhaled air increased, indicating intensification of ammonium formation in the body. Barbiturate coma did not change the slope of curves of dose-dependent increase of ammonium or urea levels in the blood of rats injected with ammonium acetate, which attested to the absence of appreciable disorders in the ammonium detoxifying function of the liver. Ammonium hyperproduction could be caused by gastrointestinal stasis verified by X-ray examination and confirmed by correlation between blood urea level and stool retention in narcotized rats.

Effects of Cyclophosphamide and Lactulose on the Release of Ammonia and Medium-Molecular-Weight Substances from the Intestine into Blood in Rats

“…Because of CP enterotoxicity [6], substances formed in the intestinal chyme, including compounds of low (<300 g/mole) and medium (300-5000 g/mole) molar weight (MMWS), may be involved in the formation of these effects. We have confi rmed previously this hypothesis for one of the low molar weight substance -ammonia [4,5]. Lactulose is prescribed for hepatic encephalopathy in order to suppress toxigenic and ammonia-producing microfl ora in the intestinal lumen [3].…”