一氧化氮在新生鼠缺氧缺血性脑损伤中的变化及高压氧的治疗机制

目的 探讨围产期缺氧缺血引起新生鼠脑损伤后脑组织一氧化氮(NO)含量的变化,以及高压氧(HBO)干预治疗的机制.方法 结扎孕鼠双侧子宫动脉复制围产期缺氧缺血性脑损伤(HIBD)的动物模型,并于生后6h、24h、72h、7d断头取脑,测定NO含量变化及一氧化氮合酶(NOS)的表达,应用TUNEL染色观察细胞凋亡的变化,设立对照组及HBO干预组.结果 HIBD后NO水平有明显上升,NOS表达增强,随缺氧时间的延长而增强,并伴有凋亡细胞显著增加.HBO治疗后可降低脑组织NOS的表达及NO的水平,明显减轻了脑细胞的凋亡.结论 在HIBD时存在NO的过量生成,NO参与HIBD的病理过程,HBO保护损伤脑组织的治疗机制可能与抑制NO生成有关.

Abstract：

Objective To examine the dynamic variation of plasma nitric oxide (NO) level in newborn rats with hypoxic isehemie brain damage (HIBD) and their relation with hyperbaric oxygen (HBO) treatment. Methods To produce HIBD animal model by ligating the uterine arteries of pregnant rats. We detected the plasma NO level and nitric oxide synthetase (NOS) expression by radioimmunoassay and immunohistochemistry before operation and 6h, 24h, 72h,7d after HIBD and treatment with HBO. The pattern of neuronal cell death after HIBD was examined using TUNEL staining. Results Plasma NO level markedly elevated at 24h after HIBD, and NOS expression reached peak at 72h. The two parameters were significantly fell in the same groups treated with HBO. HBO also minimized eminently apoptosis of cerebral cells.Conclusions HIBD may be associated with the abnormal excretion of NO, and the mechanism of HBO treatment of newborn rats with HIBD may be associated with the reduction of plasma NO.

Dynamic variation of plasma nitric oxide levels in newborn rats with hypoxic ischemic brain damage and their relation with hyperbaric oxygen treatment

Objective To examine the dynamic variation of plasma nitric oxide (NO) level in newborn rats with hypoxic isehemie brain damage (HIBD) and their relation with hyperbaric oxygen (HBO) treatment. Methods To produce HIBD animal model by ligating the uterine arteries of pregnant rats. We detected the plasma NO level and nitric oxide synthetase (NOS) expression by radioimmunoassay and immunohistochemistry before operation and 6h, 24h, 72h,7d after HIBD and treatment with HBO. The pattern of neuronal cell death after HIBD was examined using TUNEL staining. Results Plasma NO level markedly elevated at 24h after HIBD, and NOS expression reached peak at 72h. The two parameters were significantly fell in the same groups treated with HBO. HBO also minimized eminently apoptosis of cerebral cells.Conclusions HIBD may be associated with the abnormal excretion of NO, and the mechanism of HBO treatment of newborn rats with HIBD may be associated with the reduction of plasma NO.