[Role of cerebral nitrogen metabolism in the mechanisms of the therapeutic action of oxygen under elevated pressure in hemorrhagic shock].
The hyperbaric oxygen therapy (3 ata O2, 60 min exposure) of hemorrhagic shock in cats (arterial pressure--60/50 mm Hg) prevents a sharp increase of ammonia, urea, alanin, gamma-aminobutyric acid content in the brain, typical of oxygen deficiency, and activates glutamine formation. The processes of ammonia detoxication connected with glutamate and glutamine synthesis intensification course more intensively in the sensory-motor cortex than in the limbic brain structures.
D000409:Alanine / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002415:Cats; D005971:Glutamates / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D006931:Hyperbaric Oxygenation; D008032:Limbic System / Q000378:metabolism; D009044:Motor Cortex / Q000378:metabolism; D009584:Nitrogen / Q000378:metabolism*; D012771:Shock, Hemorrhagic / Q000378:metabolism / Q000628:therapy*; D013003:Somatosensory Cortex / Q000378:metabolism; D014508:Urea / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D005971:Glutamates; D005973:Glutamine; D005680:gamma-Aminobutyric Acid; D000641:Ammonia; D014508:Urea; D009584:Nitrogen; D000409:Alanine
Rol' azotistogo metabolizma mozga v mekhanizmakh lechebnogo deĭstviia kisloroda pod povyshennym davleniem pri gemorragicheskom shoke