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酸中毒对沙土鼠海马脑片缺氧后突触传递恢复的影响。

Effects of acidosis on the post-hypoxic recovery of synaptic transmission in gerbil hippocampal slices.

作者信息

Kamada Y, Hiramatsu K, Sakaki T

机构信息

Department of Neurosurgery, Nara Medical University, 840 Shijou-cho, Nara 634-8522, Kashihara, Japan.

出版信息

Brain Res. 2000 Jun 23;868(2):347-51. doi: 10.1016/s0006-8993(00)02286-1.

Abstract

We investigated the effects of acidosis on the hypoxic neuronal damage using gerbil hippocampal slices. Acidosis has delayed the onset of harmful hypoxic depolarization, resulting in a decrease in the total hypoxic period and the hypoxic depolarization. This effect has been considered to be protective. However, the synaptic recovery after reoxygenation was attenuated when acidosis (pH: 6.2-6.9) was sustained. Conversely, the synaptic recovery was potentiated when the acidosis was restored to the physiological milieu during the reoxygenation period. These results suggest that acidosis plays a protective effect against the hypoxic neuronal damage only when rapid appreciable pH recovery is achieved during reoxygenation.

摘要

我们使用沙鼠海马切片研究了酸中毒对缺氧性神经元损伤的影响。酸中毒延迟了有害的缺氧去极化的发生,导致总缺氧期和缺氧去极化减少。这种作用被认为具有保护作用。然而,当酸中毒(pH值:6.2 - 6.9)持续存在时,复氧后的突触恢复减弱。相反,在复氧期将酸中毒恢复到生理环境时,突触恢复得到增强。这些结果表明,只有在复氧期间实现快速且明显的pH值恢复时,酸中毒才对缺氧性神经元损伤起保护作用。

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