大剂量一氧化氮合酶抑制剂在局灶性脑缺血中对神经细胞凋亡的影响

目的：研究一氧化氮(NO)在局灶性脑缺血再灌流过程中对神经细胞的作用机制及NO与细胞凋亡的关系。方法：利用光镜、电镜观察N-硝基-左旋-精氨酸（N-nitro-L-arginine，NNLA）干预后局灶脑缺血大鼠脑组织的病理学改变。结果：大剂量给予NNLA干预后，手术侧电镜下半影区神经细胞改变较手术对照组明显，神经细胞核周水肿、溶解和小胶质细胞核染色质凝集，以细胞坏死为主。结论：过多的NO可能通过两种方式导致神经细胞损伤，其一是过量NO以活性氧自由基(ROS)表达式直接攻击神经细胞，是神经细胞损伤的直接毒性分子。其二是过少的NO不足以维持脑血管的基础张力，脑血流下降，导致缺氧，引起神经细胞损伤。

Effect of high dose NOS inhibitor on neurone apoptosis in focal cerebral ischemia

ObjectiveTo study the relationship between nitric oxide (NO) and apoptosis in the focal cerebral ischemia. MethodsUsing light microscope and electric microscope,the pathological changes of cerebral in the focal cerebral ischemia were observed. ResultsWhen the focal cerebral ischemia in rats was influenced by high dose N nitro L arginine ( NNLA ), the operation side brain appeared edema around nucleus, dissolutuin and distortion of neuronal cell nucleus in a part of hippocampus CA4 region and cortex region. These changes under hight microscope were more obvious than that in operation control group. Under electric microscope, the changes of the organelles of neuronal cell nucleus and chromatin dense stain of gliocyte nucleus in ischemic penumbra were found. ConclusionExcessive NO has two forms to induce neuron injury. First,excessive NO is a reactive oxygen species (ROS). It may attack straightly to nerves and vascular endothelial cell and is a direct toxicity molecule. Second, the lack of NO can not keep the cerebrovasurlar basic tension. It may induce the decrease of cerebral blood flow and anoxia and neuron injury.