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目的研究ATP敏感性K+通道阻断剂glipizide（GLI）对缺氧后海马脑片损伤以及海马神经元[Ca(2+)]i变化的影响。方法以大鼠离体海马脑片和体外分散培养的海马神经元为标本，分别采用电生理微电极记录技术以及激光扫描共聚焦显微镜监测神经元[Ca(2+)]i的方法。结果预先用GLI（20μmol／L）灌流的海马脑片缺氧后PV持续时间较对照组显著缩短，提示其加重了海马不可逆缺氧损伤的发生；另外急性缺氧可诱导海马神经元[Ca(2+)]i迅速升高，而预先加入GLI（20μmol／L）能显著加剧[Ca(2+)]i的升高程度。结论ATP敏感性K+通道在缺氧过程中的开放对大鼠海马脑区具有重要的保护作用，它可显著降低缺氧所致神经元[Ca(2+)]i升高，提高海马脑片的抗缺氧能力。这可能是其对抗海马缺氧损伤的主要作用机制之一。
Aim To investigate the effect of glializide (GLI), an ATP sensitive K + channel blocker, on the injury of hippocampal slices and the change of [Ca (2 +)] i in hippocampal neurons after hypoxia. Methods Rat hippocampal slices and hippocampal neurons dispersed in vitro were used as samples to detect neuronal [Ca (2 +)] i by electrophysiological microelectrode recording and laser scanning confocal microscopy. Results The hippocampal slices perfused with GLI (20μmol / L) significantly delayed the duration of PV after hypoxia compared with the control group, suggesting that it increased the irreversible hypoxia injury in the hippocampus. In addition, acute hypoxia could induce the hippocampal neuron [Ca 2 +)] i increased rapidly, while pretreatment with GLI (20μmol / L) significantly increased the level of [Ca (2 +)] i. Conclusion The opening of ATP-sensitive K + channels during hypoxia plays an important protective role in the hippocampus of rats. It can significantly reduce the increase of [Ca (2 +)] i in hippocampal neurons induced by hypoxia, Anti-hypoxia ability. This may be one of its main mechanisms of action against hypoxic injury in the hippocampus.