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局灶性脑缺血引起的细胞外氨基酸神经递质变化。

Changes in extracellular amino acid neurotransmitters produced by focal cerebral ischemia.

作者信息

Graham S H, Shiraishi K, Panter S S, Simon R P, Faden A I

机构信息

Department of Neurology, University of California, San Francisco.

出版信息

Neurosci Lett. 1990 Mar 2;110(1-2):124-30. doi: 10.1016/0304-3940(90)90799-f.

Abstract

Excitatory amino acids (EAAs) have been implicated in the pathophysiology of cellular injury after brain ischemia. Changes in extracellular levels of amino acids in rat cerebral cortex after permanent proximal middle cerebral artery (MCA) occlusion were examined using microdialysis. Significant increases were found in dialysate concentrations of glutamate, aspartate and gamma-aminobutyric acid (GABA) from the ischemic cortex during the first 90 min after MCA occlusion compared to pre-ischemic concentrations and contralateral hemispheric controls. Total tissue levels of these amino acids in the infarcted hemisphere 90 min after onset of ischemia were not different from the contralateral hemisphere. These results are consistent with the hypothesis that the release of EAAs may contribute to tissue damage in focal cerebral ischemia.

摘要

兴奋性氨基酸(EAAs)与脑缺血后细胞损伤的病理生理学有关。采用微透析法检测大鼠大脑中动脉(MCA)近端永久性闭塞后大脑皮质细胞外氨基酸水平的变化。与缺血前浓度和对侧半球对照相比,MCA闭塞后最初90分钟内,缺血皮质透析液中谷氨酸、天冬氨酸和γ-氨基丁酸(GABA)的浓度显著升高。缺血发作90分钟后,梗死半球这些氨基酸的总组织水平与对侧半球无差异。这些结果与以下假设一致,即兴奋性氨基酸的释放可能导致局灶性脑缺血中的组织损伤。

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