Simpson R E, Walter G A, Phillis J W
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Neurosci Lett. 1991 Mar 11;124(1):83-6. doi: 10.1016/0304-3940(91)90827-g.
The effects of systemic hypothermia (33.5 degrees C) on the ischemia-evoked release of the neurotransmitter amino acids, glutamate, aspartate, gamma-amino-butyric acid (GABA) and glycine into rat cerebral cortical superfusates were evaluated in the rat four vessel occlusion model. Glutamate, aspartate and GABA, but not glycine, levels were enhanced during and following a 20 min period of ischemia. However, when compared with normothermic ischemic animals, no reductions in glutamate, aspartate or GABA levels in the superfusates were apparent either prior to, during or following forebrain ischemic episodes. Indeed, the superfusate levels of aspartate and GABA were transiently increased immediately following ischemia. Glycine levels were significantly depressed, both pre- and post-ischemia, in cortical superfusates from hypothermic animals in comparison with normothermic rats.
在大鼠四血管闭塞模型中，评估了全身低温（33.5摄氏度）对神经递质氨基酸（谷氨酸、天冬氨酸、γ-氨基丁酸（GABA）和甘氨酸）缺血诱发释放到大鼠大脑皮质灌流液中的影响。在20分钟缺血期间及之后，谷氨酸、天冬氨酸和GABA水平升高，但甘氨酸水平未升高。然而，与正常体温缺血动物相比，在前脑缺血发作之前、期间或之后，灌流液中谷氨酸、天冬氨酸或GABA水平均无明显降低。事实上，缺血后立即天冬氨酸和GABA的灌流液水平短暂升高。与正常体温大鼠相比，低温动物皮质灌流液中甘氨酸水平在缺血前后均显著降低。
