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.
Subject(s)
Coma/blood , Coma/complications , Hyperammonemia/etiology , Ammonia/blood , Animals , Coma/chemically induced , Coma/physiopathology , Female , Gastrointestinal Motility/drug effects , Hyperammonemia/blood , Hyperammonemia/physiopathology , Rats , Thiopental/toxicityABSTRACT
In rats with experimental thiopental coma rectal temperature decreased by 9.4 degrees C, oxygen consumption 5-fold, and arteriovenous Po(2)gradient decreased 2-fold within 3 h; CO(2)accumulated in the blood and mixed type acidosis developed. Administration of sodium succinate under these conditions increased arteriovenous Po(2)gradient and reduced manifestations of metabolic acidosis. Maintenance of normal body temperature (warming) corrected primarily manifestations of respiratory acidosis. Each therapeutic agent reduced inhibition of O(2)consumption by 1/4; animal survival tended to increase from 42 to 50%. Combined use of these treatments potentiated the antiacidotic effect and increased survival to 92%. The authors conclude that hypothermia inhibits the therapeutic effect of succinate in barbiturate coma.
Subject(s)
Acidosis, Respiratory/etiology , Body Temperature/physiology , Coma/drug therapy , Succinates/therapeutic use , Thiopental/toxicity , Acidosis, Respiratory/drug therapy , Animals , Body Temperature/drug effects , Carbon Dioxide/blood , Coma/chemically induced , Coma/complications , Female , Oxygen/blood , Oxygen Consumption/drug effects , Rats , Succinates/pharmacology , Time FactorsABSTRACT
Krebs cycle intermediates normalized gas exchange and decreased the mortality rate in rats with barbiturate coma. Treatment with other substrates including glucose and products of glycolysis was ineffective. Oxygen inhalation had no effect on oxygen consumption and indexes of external respiration. Our results suggest that deficiency of endogenous intermediates of the Krebs cycle, but not disturbances in oxygen mass transfer, serves as a limiting factor for oxygen consumption in rats with barbiturate coma.
Subject(s)
Coma/metabolism , Oxygen Consumption/drug effects , Thiopental/poisoning , Animals , Citric Acid Cycle/physiology , Coma/chemically induced , Coma/therapy , Female , Oxygen/metabolism , Oxygen Inhalation Therapy , Rats , Succinates/pharmacologyABSTRACT
Injection of sodium succinate in doses of 5 or 10 mmol/kg (but not 1 mmol/kg) intensified oxygen consumption in rats with sodium thiopental-induced coma. Injection of SDH inhibitor (sodium malonate) inhibited gas exchange and abolished the effect of sodium succinate. The effect of succinate on rat survival was positive, while that of malonate was negative, but manifested only as a trend. The critical role of succinate oxidation in preventing lethal complications of barbiturate-induced coma is proved.
