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Catecholamines in Experimental Brain Ischemia
Kyuya Kogure, MD;
Peritz Scheinberg, MD;
Akira Matsumoto, MD;
Raul Busto;
Oscar M. Reinmuth, MD
Arch Neurol. 1975;32(1):21-24.
Abstract
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Local cerebral ischemia was produced in rats by internal carotid artery injection of 35µ 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 vasoconstriction that follows embolization. Dopamine changes are a reflection of alterations in energy metabolism.
Author Affiliations
From the Cerebral Vascular Disease Research Center, Department of Neurology, University of Miami School of Medicine, Miami, Fla.
Footnotes
Accepted for publication June 24, 1974.
Reprint requests to Department of Neurology, University of Miami School of Medicine, PO Box 520875 Biscayne Annex, Miami, FL 33152 (Dr. Scheinberg).
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