摘要
目的 观察急性低压缺氧对老龄大鼠脑组织中内皮素 (ET)、一氧化氮 (NO)含量和大脑皮质光、电镜形态学的影响以及神经节苷脂的防治作用。 方法 40只 2 2月龄 Wistar大鼠随机分成生理盐水对照组、生理盐水缺氧组和神经节苷脂缺氧组。急性低压缺氧 (80 0 0 m,30 m in)前 4h各组均腹腔注射相同体积的生理盐水或神经节苷脂 (GM1 ) ,测定各组大脑皮质和丘脑匀浆中 ET、NO的含量 ,观察大脑皮质光、电镜形态学的改变。 结果 急性低压缺氧后大鼠大脑皮质和丘脑中 ET、NO含量明显升高 (P<0 .0 1或 P<0 .0 5 ) ,大脑皮质发生水肿、变性等损害。GM1 缺氧组 ET、NO含量较生理盐水缺氧组明显下降 (P<0 .0 5 ) ,大脑皮质缺氧性损害明显减轻。 结论 急性低压缺氧可引起老龄大鼠大脑皮质和丘脑中 ET、NO含量明显升高以及大脑皮质血管内皮细胞和神经细胞明显损伤 ,ET、NO可能参与了缺氧性脑损害的病理过程。GM1 对老龄大鼠缺氧性脑损害有一定的早期防治作用。
Objective To observe the effect of acute hypoxia on endothelin(ET) and nitric oxide (NO) contents and ultrastructure changes of cerebral cortex in old rats and the protective effect of ganglioside GM 1. Methods Forty 22 month old Wistar rats were divided into normal saline(NS) control group, NS hypoxia group, and ganglioside GM 1 hypoxia group. Ganglioside GM 1(35 mg/kg,i.p.) or NS was given 4 h before entering hypobaric chamber and acute hypoxia exposure (8 000 m ,30 min).The ET and NO contents of cerebral cortex and thalamus were measured and the microscopic and electron miscropic changes of cerebral cortex were examined. Results The ET and NO contents of cerebral cortex and thamulus in NS hypoxia group were significantly higher than those in NS control group ( P<0.01,P <0.05). The ultrastructural changes of cerebral cortex capillaries, perivascular tissue and feltwork in NS control group were prominent, while the changes in GM 1 hypoxia group were not significant as compared with control's. Conclusion It is suggested that, the increase of ET and NO contents of cerebral cortex and thalamus may participate in the pathogenesis of hypoxia brain injury in old rats.Administration of GM 1 before acute hypoxia exposure may protect the old rats from brain injury.
出处
《中华航空航天医学杂志》
CSCD
2000年第1期36-38,共3页
Chinese Journal of Aerospace Medicine
