Stroke, Vol 19, 1540-1543, Copyright © 1988 by American Heart Association
T Kawano, K Tsutsumi, H Miyake and K Mori
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.
ARTICLES
Striatal dopamine in acute cerebral ischemia of stroke-resistant rats
Department of Neurosurgery, Nagasaki University School of Medicine, Japan.
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