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Stroke. 1988;19:1540-1543

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Stroke, Vol 19, 1540-1543, Copyright © 1988 by American Heart Association


ARTICLES

Striatal dopamine in acute cerebral ischemia of stroke-resistant rats

T Kawano, K Tsutsumi, H Miyake and K Mori
Department of Neurosurgery, Nagasaki University School of Medicine, Japan.

We devised the present experiments to assess the effects of ischemia on the production of dopamine in the caudate nucleus of spontaneously hypertensive stroke-resistant rats. Ringer's solution was continuously perfused at a rate of 10 microliters/min through 0.2-mm-diameter dialysis tubing implanted in the rat's caudate nucleus. After bilateral occlusion of the common carotid artery, perfusate was collected at 20- minute intervals for 120 minutes and was analyzed for monoamines and their metabolites using high-performance liquid chromatography and an electrochemical detection system. The extracellular concentration of dopamine increased abruptly approximately 3 minutes after the ischemic insult, reached a maximum at between 20 and 40 minutes after the insult, and subsequently decreased. During the 120 minutes, 3,4- dihydroxyphenylacetic acid and 5-hydroxyindole-3-acetic acid concentrations decreased significantly, whereas 5-hydroxytryptamine was not detected. Our results indicate that during cerebral ischemia a large increase in extracellular dopamine concentration in the caudate nucleus occurs, probably as a result of energy failure of the cell membranes. This leakage of dopamine may be a causal factor in the neuronal damage associated with cerebral ischemia.