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pubmed:abstractText |
14C-acetate is preferentially taken up by astrocytes, and is a useful tool for measurement of glial metabolism. The aim of this study was to determine the effects of short-term ischemia on 14C-acetate uptake in the rat brain. The middle cerebral artery was occluded for 3, 10, or 30 minutes. Five minutes after reperfusion, rats were injected with 14C-acetate and decapitated 5 minutes later. Radioactivity concentrations in striatum and cerebral cortex were determined by autoradiography. Cerebral blood flow was also measured using 14C-iodoamphetamine. Neuronal cell death was measured by Nissl staining, and expression of monocarboxylate transporter-1 was examined by immunohistochemical staining. A significant reduction of 14C-acetate uptake was observed in striatum by 3 minutes of occlusion. The degree of reduction of 14C-acetate uptake and reduction area were increased with occlusion period. In contrast, within the same region the regional blood flow was increased by 10 minutes of occlusion, suggesting that uptake of 14C-acetate was independent of blood flow. No neural cell death was detected, and no significant alteration of monocarboxylate transporter-1 expression was observed by 30 minutes of occlusion. These results indicate that 14C-acetate uptake is a sensitive marker for glial metabolism in the ischemic rat brain.
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