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Dynamic regional changes of extracellular ascorbic acid during global cerebral ischemia: studied with in vivo microdialysis coupled with on-line electrochemical detection.

作者信息

Liu Kun, Lin Yuqing, Yu Ping, Mao Lanqun

机构信息

Beijing National Laboratory for Molecular Sciences, Institute of Chemistry, the Chinese Academy of Sciences, Beijing, China.

出版信息

Brain Res. 2009 Feb 9;1253:161-8. doi: 10.1016/j.brainres.2008.11.096. Epub 2008 Dec 11.

DOI:10.1016/j.brainres.2008.11.096
PMID:19100721
Abstract

The morphologic and functional outcomes of cerebral ischemia generally result from the acute neurochemical changes that occur 1 h after cerebral ischemia. As one of the small chemical species, ascorbic acid (AA) is involved in almost all kinds of neurochemical processes in acute cerebral ischemia. To understand the neurochemical processes in global cerebral ischemia, this study compares the dynamic regional changes of extracellular AA level, with in vivo microdialysis coupled with on-line electrochemical detection, in four different brain regions, 1 h after global cerebral ischemia induced by two-vessel occlusion (2-VO). The regional distribution of physiological AA levels in the microdialysates from striatum, cortex, dorsal hippocampus, and ventral hippocampus were 2.97 +/- 0.06, 3.98 +/- 0.09, 3.02 +/- 0.47, and 3.80 +/- 0.29 microM, respectively. In 1 h after 2-VO cerebral ischemia, the microdialysate AA levels in the above four regions varied in a different manner; the striatum AA slowly decreased to 86.49 +/- 5.53% of the basal level (n=3, P<0.05). The AA levels in the cortex, dorsal hippocampus, and ventral hippocampus increased to 549.80 +/- 167.86 % (n=3, P<0.05), 167.81 +/- 41.85 % (n=4, P<0.05) and 261.24 +/- 65.00% (n=3, P<0.05), in relation to their respective basal levels, respectively. The recorded spatiotemporal regional changes in the extracellular AA levels essentially reflect the intricate neurochemical changes during the acute period of global cerebral ischemia and may thus be useful for understanding the neurochemical processes of global cerebral ischemia.

摘要

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