Succinate and artificial maintenance of normal body temperature synergistically correct lethal disorders in thiopental coma rat

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

doi:10.1016/j.tox.2005.09.006

Toxicology

2006

DOI: 10.1016/j.tox.2005.09.006

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Succinate and artificial maintenance of normal body temperature synergistically correct lethal disorders in thiopental coma rat

Ju. Ju. Ivnitsky

V. L. Rejniuk

Timur V Schäfer

et al.

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Cited by 3 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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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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Hyperammoniemia in rats with barbiturate coma

et al. 2007

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Fulminant hyperammonaemia induced by thiopental coma in rats

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Succinate and succinate dehydrogenase as a «foothold» in the Krebs cycle in critical conditions

Orlov

Бутров

Sviridov

et al. 2023

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Purpose. Search and presentation of data from experimental and clinical studies reflecting the central role of succinate and succinate dehydrogenase in the regulation of adaptation mechanisms in critical conditions. Material and methods. The search for literature sources was carried out using the electronic resources of the Russian scientific electronic library eLIBRARY.ru, with the use of the following keywords: «Krebs cycle, succinate, succinate dehydrogenase, critical conditions», as well as in the English-language text database of medical and biological publications on medical sciences PUBMED, where similar keywords «Krebs cycle, succinate, succinate dehydrogenase, critical conditions» were used. Results. Taking into account the data presented in the review, it can be stated that the complex of succinate and succinate dehydrogenase is the central link in the Krebs cycle and the main structure of the antihypoxic ensemble of all body cells during the adaptation period under critical conditions. Conclusion. The data of experimental and clinical studies reflecting the central role of succinate and succinate dehydrogenase not only in the mechanisms of adaptation to hypoxia, but also in the regulation of inflammation, thermogenesis, hemostasis disorders, acid-base state, electrolyte metabolism, vascular tone and trophism of intestinal tissues, as well as in immunological reactions of the body, allow us to consider the substrate and enzyme as the central link of the Krebs cycle and the main structure of the antihypoxic ensemble of all body cells. The data presented in the review open up new prospects for the use of succinates in critical conditions.

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Succinate and artificial maintenance of normal body temperature synergistically correct lethal disorders in thiopental coma rat

Cited by 3 publications

References 14 publications

Hyperammoniemia in rats with barbiturate coma

Hyperammoniemia in rats with barbiturate coma

Fulminant hyperammonaemia induced by thiopental coma in rats

Succinate and succinate dehydrogenase as a «foothold» in the Krebs cycle in critical conditions

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