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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Hypoglycemia, hypoxia, and ischemia in a corticostriatal slice preparation: electrophysiologic changes and ascorbyl radical formation.
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Hypoglycemia, hypoxia, and ischemia in a corticostriatal slice preparation: electrophysiologic changes and ascorbyl radical formation.

机译：皮质口骨切片制品中的低血糖，缺氧和局部缺血：电生理变化和抗坏血酸基的形成。

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摘要

Experimental and clinical data suggest that oxygen and/or glucose deprivation alters electrical transmission in the brain and generates free radicals, which may mediate neuronal death. We have analyzed the effects of oxygen and/or glucose deprivation on both excitatory transmission, by measuring field potential amplitude, and free radical production, by using electron spin resonance (ESR) spectroscopy, in a corticostriatal slice preparation. Combined oxygen and/or glucose deprivation (ischemia) lasting 10 to 20 minutes induced a long-term depression of field potential amplitude. The ascorbyl radical could only be detected in brain slices during the reperfusion-phase after 30 minutes of ischemia. It appeared in the early minutes after the washout of ischemic medium and remained stable throughout the reperfusion phase. This radical was never detected in the external medium. Ischemia induced only a slight, but progressive, release of lactate dehydrogenase (LDH) into the external medium during the reperfusion phase. In contrast, exposure of slices to hypoxia or hypoglycemia alone resulted in transient depression of field potential amplitude, and no generation of ascorbyl radicals was observed on reperfusion. We propose that the long-lasting loss of electrical signals is the early sign of neuronal damage during ischemia. On the other hand, ascorbyl radical formation may be considered an indicator of neuronal injury after prolonged energy deprivation.
机译：实验和临床数据表明，氧和/或葡萄糖的剥夺会改变大脑中的电传递并产生自由基，这可能介导神经元死亡。我们已经通过测量场电位振幅和通过使用电子自旋共振（ESR）光谱，在皮层皮质切片制备中测量了氧和/或葡萄糖剥夺对兴奋性传输的影响。持续10到20分钟的缺氧和/或葡萄糖合并剥夺（缺血）可导致长期降低场电位振幅。抗坏血酸自由基只能在缺血30分钟后的再灌注阶段在脑片中检测到。它出现在缺血介质冲洗后的早期，并在整个再灌注阶段保持稳定。在外部介质中从未发现过这种自由基。在再灌注阶段，局部缺血仅诱导乳酸脱氢酶（LDH）轻微但逐渐释放。相反，仅将切片暴露于低氧或低血糖会导致场电位振幅短暂下降，并且在再灌注时未观察到抗坏血酸自由基的产生。我们提出，电信号的长期丢失是缺血期间神经元损害的早期迹象。另一方面，抗坏血酸自由基的形成可以被认为是长时间能量缺乏后神经元损伤的指标。

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