Brain energy metabolism and catecholaminergic activity in hypoxia, hypercapnia and ischemia.
A brief review is given of recent results which indicate that several stressful situations are accompanied by an increase in cerebral metabolic rate, mediated by extrinsic or intrinsic catecholamines. These situations include withdrawal of nitrous oxide supply in paralyzed animals ("immobilization stress"), amphetamine intoxication, hypoxia, and hypercapnia. Studies of hypercapnia (and hypoxia) suggest that activity in cerebral noradrenergic systems is enhanced by cellular acidosis. Data obtained during recirculation, following severe, transient ischemia, indicate that in spite of a general depression of cerebral metabolism (and neuronal function) some neuronal systems, notably the noradrenergic ones, show evidence of increased activity.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism; D004837:Epinephrine / Q000378:metabolism; D006935:Hypercapnia / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D012701:Serotonin / Q000378:metabolism
D012701:Serotonin; D009638:Norepinephrine; D004837:Epinephrine