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夹闭大鼠双侧颈总动脉２ｈ后，对海马ＣＡ１区进行免疫电镜观察。可见实验组ＣＡ１区部分锥体细胞的胞核固缩、核染色质溶解、细胞器减少或消失；部分神经纤维的髓鞘显示轻度变性图像；部分神经末梢变性；星形胶质细胞突起肿胀；小胶质细胞活跃并包裹断离的髓鞘；生长抑素免疫反应阳性神经末梢比对照组显著增多，生长抑素阳性轴突可与阴性树突形成轴一树突触。以上结果提示：缺血可导致海马ＣＡ１区神经元发生不同程度的损伤和胶质细胞反应，继而引起生长抑素神经元的反馈性兴奋，释放生长抑素增多，刺激存活的锥体细胞，使之兴奋，从而参与脑缺血的发病过程。
After occlusion of bilateral common carotid arteries in rats for 2 hours, the hippocampal CA1 region was observed by immunoelectron microscopy. In the experimental group, some pyramidal cells in pyramidal cells of CA1 area were pyknotic, nuclear chromatin was dissolved, and organelles were reduced or disappeared; myelin sheaths of some nerve fibers showed mild degeneration images; some degeneration of nerve endings; swelling of astrocytes; Microglial cells were active and wrapped myelin sheath off; somatostatin immunoreactive positive nerve endings significantly increased compared with the control group, somatostatin-positive axons can form a axonal dendrites with the negative dendrites. The above results suggest that: ischemia can cause neurons in the hippocampal CA1 area varying degrees of damage and glial response, which in turn leads to the somatostatin neurons feedback excitement, the release of somatostatin to stimulate the survival of the pyramidal cells, The excitement, which involved in the pathogenesis of cerebral ischemia.