[Effect of gamma-oxybutyrate on energy metabolism and the cyclic nucleotide level in nerve tissue in experimental intracerebral hemorrhage].
Experimental intracerebral hemorrhage (EICH) was shown to cause a disorder of the functional state of the brain mitochondria. The rate of oxidation of NAD- and FAD-linked substrates in 3 and 4 states decreased 1 and 24 hours after hemorrhage. An injection of gamma-hydroxybutyrate 1 hour before decapitation increased the rate of mitochondrial respiration. EICH was found to increase cGMP level and to decrease cAMP level. A combined action of hemorrhage and gamma-hydroxybutyrate produced a greater lowering of cAMP level and an elevation of cGMP level.
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002543:Cerebral Hemorrhage / Q000188:drug therapy* / Q000378:metabolism; D004353:Drug Evaluation, Preclinical; D004734:Energy Metabolism / Q000187:drug effects*; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009417:Nerve Tissue / Q000187:drug effects* / Q000378:metabolism; D009712:Nucleotides, Cyclic / Q000378:metabolism*; D051381:Rats; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use
D009712:Nucleotides, Cyclic; D005680:gamma-Aminobutyric Acid; C009338:succinic semialdehyde
Vliianie gamma-oksibutirata na énergeticheskiĭ metabolizm i uroven' tsiklicheskikh nukleotidov v nervnoĭ tkani pri éksperimental'nom vnutrimozgovom krovoizliianii.