[Bioenergetic processes in the cerebral cortex and diensephalon during hyperbaric oxygenation therapy of acute blood loss].
It has been demonstrated in experiments on 134 cats that during acute blood loss (24 +/- 0.8 ml/kg), hyperbaric oxygen therapy (3039 hPa, 60 min) stimulates cytochrome oxidase, eliminates compensatory activation of mitochondrial creatine kinase and maintains the hyperactivity of cytoplasmic creatine kinase in the diencephalon, stabilizes the elevated AMP content at the level of blood loss compensation stage, prevents the fall in pO2 and in the ATP level as well as that in the energy charge and creatine phosphate content in the sensomotor cortex and subcortex, that is typical for the decompensation stage. Besides, hyperbaric oxygen therapy also averts the development of the terminal state that supervenes in the majority of untreated animals.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000740:Anemia / Q000628:therapy*; D000818:Animals; D001815:Bloodletting; D017301:Ca(2+) Mg(2+)-ATPase; D002415:Cats; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism; D005260:Female; D006931:Hyperbaric Oxygenation; D007031:Hypothalamus / Q000378:metabolism*; D008297:Male; D010725:Phosphocreatine / Q000378:metabolism; D013003:Somatosensory Cortex / Q000378:metabolism*; D013788:Thalamus / Q000378:metabolism*
D010725:Phosphocreatine; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D003576:Electron Transport Complex IV; D000251:Adenosine Triphosphatases; D017301:Ca(2+) Mg(2+)-ATPase
Bioénergeticheskie protsessy v kore i promezhutochnom mozge pri giperbaricheskoĭ kislorodnoĭ terapii ostroĭ krovopoteri.