Fulminant hyperammonaemia induced by thiopental coma in rats

Ivnitsky, Ju. Ju.; Rejniuk, V. L.; Schäfer, Timur V; Malakhovsky, Vladimir N.

doi:10.1016/j.tox.2006.04.002

Cited by 9 publications

(8 citation statements)

References 13 publications

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“…Inhibition of gas exchange and thermogenesis in barbiturate coma (BC) can be partially caused by exhaustion of the tissue pool of the Krebs cycle intermediates [2,3], which probably results from intensification of α-ketoglutarate and oxaloacetate amination under conditions of hyperammoniemia development. The content of the gastrointestinal tract serves as the main source of ammonium in the body; ammonium formation can many-fold increase within several minutes.…”

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confidence: 99%

Hyperammoniemia in rats with barbiturate coma

et al. 2007

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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.

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confidence: 99%

Hyperammoniemia in rats with barbiturate coma

et al. 2007

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“…Obviously, prevention of hypothermia gave way to recruitment of exogenous SS into the Krebs cycle, which can explain the supra-additive increase in animal survival by 49-50% (Table 1) after combined use of IR and SS in barbiturate coma. Considering previous data [2,3], we can expect further amplification of the therapeutic effect after repeated injections of SS and prolongation of IR exposure.…”

Section: Resultsmentioning

confidence: 80%

“…The intensity of cell respiration in barbiturate coma can be limited by availability of Krebs cycle intermediates and be corrected by their injection [3]. Hypothermia can inhibit the resorption of exogenous carbonic acids and their incorporation into the Krebs cycle, and therefore warming can promote their therapeutic effect.…”

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confidence: 99%

Synergism of isothermal regimen and sodium succinate in experimental therapy of barbiturate coma

2006

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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.

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“…The concentrations of NH 3 in the blood and lavage solution were evaluated by the microdiffusion method followed by acidometric titration [1,3]. The rate of NH 3 accumulation in lavage solution was estimated.…”

Section: Methodsmentioning

confidence: 99%

“…Hyperammoniemia not associated with blood concentration or inhibited urinary excretion of NH 3 or its elimination with exhaled air develops in rats during simulation of barbiturate coma [3]. Hyperammoniemia was observed against the background of gastrointestinal stasis.…”

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confidence: 93%

Intensification of ammonium diffusion from rat gastrointestinal tract during acute barbiturate intoxication

2008

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In rats with acute sodium thiopental intoxication, ammonium concentration in the caecal contents was at the lower boundary of control values, while accumulation of ammonium in lavage solution injected intraperitoneally was 50-70% accelerated. Blood ammonium level did not change 3 h after sodium thiopental injection in a dose inducing sopor, but increased 3-fold during coma modeling. Intragastric administration of gentamicin (antibiotic poorly absorbed from the gastrointestinal tract) 2-fold reduced ammonium concentration in the caecal contents and prevented hyperammoniemia during induction of barbiturate coma. Hence, increased permeability of the gastrointestinal wall for ammonium promotes the development of hyperammoniemia in rats during induction of barbiturate coma.

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Fulminant hyperammonaemia induced by thiopental coma in rats

Cited by 9 publications

References 13 publications

Hyperammoniemia in rats with barbiturate coma

Hyperammoniemia in rats with barbiturate coma

Synergism of isothermal regimen and sodium succinate in experimental therapy of barbiturate coma

Intensification of ammonium diffusion from rat gastrointestinal tract during acute barbiturate intoxication

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