Pedersen J Z, Bernardi G, Centonze D, Pisani A, Rossi L, Rotilio G, Calabresi P
Department of Biology, University of Rome Tor Vergata, Italy.
J Cereb Blood Flow Metab. 1998 Aug;18(8):868-75. doi: 10.1097/00004647-199808000-00006.
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.
实验和临床数据表明，氧和/或葡萄糖剥夺会改变大脑中的电传递并产生自由基，而自由基可能介导神经元死亡。我们通过测量场电位幅度来分析氧和/或葡萄糖剥夺对兴奋性传递的影响，并通过电子自旋共振（ESR）光谱法来分析其对自由基产生的影响，实验采用皮质纹状体脑片标本。持续10至20分钟的联合氧和/或葡萄糖剥夺（缺血）会导致场电位幅度的长期抑制。仅在缺血30分钟后的再灌注期，才可以在脑片中检测到抗坏血酸自由基。它在缺血培养基洗脱后的最初几分钟出现，并在整个再灌注期保持稳定。在外部培养基中从未检测到这种自由基。缺血仅在再灌注期导致乳酸脱氢酶（LDH）向外部培养基中轻微但持续地释放。相比之下，仅将脑片暴露于低氧或低血糖会导致场电位幅度短暂抑制，且再灌注时未观察到抗坏血酸自由基的产生。我们认为，电信号的长期丧失是缺血期间神经元损伤的早期迹象。另一方面，抗坏血酸自由基的形成可被视为长时间能量剥夺后神经元损伤的一个指标。
