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目的 :观察缺血性脑损害中一氧化氮合酶(NOS)神经元的变化规律 ,探讨一氧化氮(NO)参与缺血性脑损害的机制。方法 :采用组织化学染色方法观察大鼠局灶性脑缺血后尼克酰胺腺啶呤二核苷酸磷酸黄递酶(NADPH d)阳性神经元的变化规律。结果 :大鼠局灶性脑缺血后NADPH d阳性神经元明显增加 ,缺血2h后出现形态学改变 ,且以细胞皱缩、胞浆致密为主要死亡方式。结论 :NADPH d阳性神经元对缺血性损害相对耐受 ,细胞凋亡可能为其主要死亡方式。
Objective: To observe the changes of nitric oxide synthase (NOS) neurons in ischemic brain damage and to explore the mechanism of nitric oxide (NO) participating in ischemic brain damage. Methods: Histochemical staining was used to observe the changes of nadamide adenine dinucleotide phosphate-diaphorase (NADPH-d) positive neurons after focal cerebral ischemia in rats. Results: After focal cerebral ischemia in rats, NADPH d positive neurons increased significantly, morphological changes occurred 2 h after ischemia, and the main way of death was cell shrinkage and cytoplasm densification. Conclusion: NADPH d-positive neurons are relatively resistant to ischemic damage and apoptosis may be the main way of death.