Catecholamines in experimental brain ischemia.
Local cerebral ischemia was produced in rats by internal carotid artery injection of 35 mu carbon microspheres, and brain norepinephrine (NE), dopamine, and cyclic adenosine 3, 5-monophosphate (cAMP) were measured in embolized and intact hemispheres at intervals up to four hours. Sham-operated animals were controls. There was an instantaneous increase of cAMP. Norepinephrine was reduced within two minutes after embolization and remained low for four hours. Dopamine increased by five minutes after embolization and returned to normal after four hours. Results were qualitatively similar, but less, in the nonembolized hemisphere. Accumulation of cAMP is thought to be due to a direct effect of ischemic hypoxia and may be the initiating factor in increased glycolysis that occurs in ischemia. Decrease in NE may be secondary to its generalized release from presynaptic terminals throughout the brain and could be a factor in cortical vasocontriction that follows embolization. Dopamine changes are a reflection of alterations in energy metabolism.
D000818:Animals; D001769:Blood; D001921:Brain / Q000098:blood supply* / Q000378:metabolism; D002244:Carbon; D002245:Carbon Dioxide / Q000097:blood; D002343:Carotid Artery, Internal; D002395:Catecholamines / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism; D004734:Energy Metabolism; D006019:Glycolysis; D006863:Hydrogen-Ion Concentration; D007269:Injections, Intra-Arterial; D007511:Ischemia / Q000209:etiology / Q000378:metabolism*; D008863:Microspheres; D009638:Norepinephrine / Q000378:metabolism; D010100:Oxygen / Q000097:blood; D051381:Rats
D002395:Catecholamines; D002245:Carbon Dioxide; D002244:Carbon; D000242:Cyclic AMP; D010100:Oxygen; D004298:Dopamine; D009638:Norepinephrine