新生大鼠缺血缺氧后脑内一氧化氮合酶的动态表达

实验采用生后14天Wistar大鼠缺血缺氧（HI）动物模型。用免疫组织化学方法观察HI复苏（HI/R0后前脑一氧化氮合酶动态表达。结果显示；神经元一氧化氮合酶（nNOS)阳性神经元主要分布于新生大鼠大脑皮层的Ⅲ-Ⅳ层。尾状核，隔核及嗅结节，HI/R早期其表达水平无明显变化；复苏48小时及5天后，可分别在右侧大脑顶皮层或右侧大脑顶皮层和尾状核区出现梗塞灶，该区nNOS阳性神经元明显减少，而诱导型一氧化氮合酶（iNOS)阳性细胞在HI/R后12小时始现于损伤侧的侧脑室；随时间的推移在损伤侧缰核，皮层，尾状核以及丘脑背外侧核，丘脑腹侧核可见iNOS阳性细胞逐渐增多并染色加深，用识别单核巨噬细胞的克隆ED1单克隆抗体检测可见ED1阳性细胞出现的时间和在脑区的分布与iNOS阳性细胞相似，本实验提示，在局灶性脑缺血缺氧早期，脑内NO的释放不依赖于nNOS阳性神经元或iNOS阳性细胞，而在局灶性脑缺血缺氧晚期，iNOS阳性细胞产生的NO可能参与了脑损伤的过程。

DYNAMIC EXPRESSION OF NITRIC OXIDE SYNTHASE FOLLOWING CEREBRAL HYPOXIA-ISCHEMIA IN NEONATAL RATS

The dynamic expression of nitric oxide synthase (NOS) in the forebrain of 14 day neonatal rats was observed following cerebral hypoxia ischemia (HI) Right carotid artery ligation was performed and followed by inhalation of 8% oxygen (92% nitrogen) for 1 5 hours Immunohistochemical staining for neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) was performed at 0, 6, 12, 24, 48h and 5 days following resuscitation The results were as follows: Constitutive nNOS was expressed in the cortex, the caudate,the septic area and the olfactory tubercles of the normal neonatal brain These positively stained neurons remained detectable until 5 days following cerebral HI By day 5, the number of positive neurons decreased dramatically owing to the formation of infarction iNOS positive cells were first seen in the right ventricle 12h following resuscitation and they appeared in the right habenular nucleus and occasionally right dorsal thalamus 24h following resuscitation The number of iNOS positive cells was increased and stronger staining was seen at 48h following resuscitation in the above mentioned areas At day 5, a large amount of iNOS positive cells were seen in the right neocortex, habenular nucleus, caudate putamen and lateral-mediate thalamus as well as hippocampus Some of the iNOS positive cells showed the morphology of macrophage and mononuclear cells as well as polymorphonuclear cells Immunohistochemical staining for ED1, a clone which recognizes macrophages and monocytes showed positive cells in the areas where iNOS positive cells were seen These results indicate that nNOS positive neurons may not be involved in the over production of NO during cerebral HI, and NO released by the iNOS positive cells may not contribute to the triggering of cell death but may take part in the later phase of tissue damage following cerebral HI.