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用凝胶电泳及原位末端标记研究大鼠脑缺血再灌流后神经元的凋亡与坏死。采用可逆性大脑中动脉阻塞２ 小时，再灌流０．５～４８ 小时，造成脑缺血再灌流模型（３０ 只），用ＨＥ、原位末端标记（ＴＵＮＥＬ）和琼脂糖凝胶电泳观察神经元的改变。结果：缺血损伤区位于视前区、纹状体和皮质，再灌流０．５ 小时，视前区的缺血损伤区有较多的凋亡细胞，而皮质、纹状体仅有散在的凋亡细胞。再灌流３～６小时，凋亡细胞数量增多，并可见坏死细胞，１２小时达高峰，持续到２４ 小时，并可见凋亡细胞各种形态，凋亡细胞主要位于缺血损伤区内界，坏死细胞也增多。４８小时完全坏死区周围有成群的凋亡细胞。电泳显示涂片状背景上有明显的ＤＮＡ带。细胞凋亡参与缺血再灌流所致的神经元损伤，凋亡细胞与坏死细胞并存，细胞凋亡使梗塞区面积扩大。
Neuronal apoptosis and necrosis after cerebral ischemia and reperfusion in rats were studied by gel electrophoresis and in situ end labeling. Cerebral ischemia-reperfusion model (30 rats) was established by reversible middle cerebral artery occlusion (2 h) and reperfusion (0.5-48 h). Neurons were observed by HE, TUNEL and agarose gel electrophoresis Change. Results: The area of ischemic injury was located in the preoptic area, the striatum and the cortex. After 0.5 hour of reperfusion, the apoptotic cells in the preoptic area had more apoptotic cells, while the cortex and striatum only scattered Apoptotic cells. After 3 to 6 hours of reperfusion, the number of apoptotic cells increased, and necrotic cells were seen. The cells reached the peak at 12 hours and lasted for 24 hours. The morphological changes of apoptotic cells were observed. Apoptotic cells were mainly located in the ischemic area, necrosis Cells also increase. 48 hours completely necrotic area surrounded by clusters of apoptotic cells. Electrophoresis showed obvious DNA bands on the smear background. Apoptosis involved in the neuronal damage caused by ischemia-reperfusion, the co-existence of apoptotic cells and necrotic cells, and the apoptosis area make the area of infarct enlarged.