Fulminant hyperammonaemia induced by thiopental coma in rats
| Autor: | Jury Ju. Ivnitsky, Timur V. Schäfer, Vladimir N. Malakhovsky, Vladimir L. Rejniuk |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
medicine.medical_specialty
Time Factors Fulminant medicine.medical_treatment Intraperitoneal injection Urine Acetates Toxicology Blood Urea Nitrogen Excretion chemistry.chemical_compound Ammonia Internal medicine medicine Animals Hyperammonemia Hypnotics and Sedatives Coma Thiopental Defecation Creatinine Dose-Response Relationship Drug Gastrointestinal Contents Rats Gastrointestinal Tract Endocrinology Sodium thiopental chemistry Urea medicine.symptom Injections Intraperitoneal Intestinal Obstruction medicine.drug |
| Zdroj: | Toxicology. 224:184-190 |
| ISSN: | 0300-483X |
| DOI: | 10.1016/j.tox.2006.04.002 |
| Popis: | 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 LD50 (but not 0.8 LD50) of sodium thiopental three times in 3 h and five times in 18 h. 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. |
| Databáze: | OpenAIRE |
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