[Mechanism of disorders in energy formation in acute hepatic ischemia].
Respiration of hepatic mitochondria of rats after addition of ischemic toxin to the incubation medium was compared with respiration of mitochondria isolated from an ischemic rat liver. Its change could be prevented in both cases by the preliminary administration of dithiotreitol and could be decreased by the subsequent addition of cytochrome C or dithiotreitol into the incubation medium. Similarity of the mechanisms of disturbed energy formation in vivo and in vitro is supposed.
D000208:Acute Disease; D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology; D003574:Cytochrome c Group / Q000494:pharmacology; D004229:Dithiothreitol / Q000494:pharmacology; D004347:Drug Interactions; D004734:Energy Metabolism; D066298:In Vitro Techniques; D007511:Ischemia / Q000378:metabolism*; D008099:Liver / Q000098:blood supply*; D008930:Mitochondria, Liver / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D014118:Toxins, Biological / Q000302:isolation & purification / Q000494:pharmacology*
D003574:Cytochrome c Group; D014118:Toxins, Biological; D000249:Adenosine Monophosphate; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D004229:Dithiothreitol
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