eNOS解偶联对减压病大鼠肺动脉内皮功能损伤的影响

发布时间：2018-02-03 10:14

本文关键词： 减压病一氧化氮合酶Ⅲ型超氧阴离子 -硝基酪氨酸　出处：《解放军医学杂志》2015年06期 　论文类型：期刊论文

【摘要】：目的探讨不安全减压对大鼠肺动脉内皮功能的影响及其相关机制。方法 60只雄性SD大鼠随机分为对照组(n=30)和减压病(DCS)组(n=30)。将DCS组大鼠置于加压舱内,暴露于600k Pa压缩空气环境下60min,再以100k Pa/min减至常压,制作DCS模型。DCS组存活大鼠及对照组大鼠麻醉后剥离肺动脉,检测离体肺动脉内皮依赖的血管舒张能力,采用Western blotting检测肺动脉组织中内皮型一氧化氮合酶(e NOS)表达情况及其解离情况,以及肺动脉组织中各蛋白硝基化水平,行离体肺动脉超氧化物阴离子探针(DHE)染色检测活性氧(ROS)形成情况。结果 DCS组30只大鼠经历不安全减压后死亡10只,存活大鼠肺动脉内皮依赖的血管舒张能力明显下降(P0.05)。DCS组及对照组e NOS表达量差异无统计学意义(P0.05),但DCS组e NOS单体/二聚体比例明显高于对照组(P0.05);DCS组肺动脉组织各蛋白酪氨酸硝基化水平明显高于对照组(P0.05)。DHE染色结果显示,DCS组肺动脉中ROS生成量明显高于对照组(P0.05)。结论模拟潜艇逃生过程中不安全减压可导致肺动脉内皮中e NOS二聚体解偶联,解离的e NOS单体不能合成NO,从而影响血管内皮依赖舒张能力;e NOS单体可促进ONOO 合成,导致肺动脉组织中蛋白酪氨酸硝基化水平提高,引起细胞信息调控紊乱,e NOS单体还可引起活性氧离子ROS形成增加,从而介导过氧化损伤。
[Abstract]:Objective to investigate the effects of unsafe decompression on pulmonary artery endothelial function in rats and its related mechanisms. Methods 60 male SD rats were randomly divided into control group (n = 30) and decompression sickness group (DCS) (n = 60). The rats in DCS group were placed in pressure chamber. Exposed to 600kPa compressed air for 60min, then reduced to atmospheric pressure by 100k Pa/min. To make DCS model. The isolated pulmonary artery endothelium dependent vasodilation ability was detected by stripping the pulmonary artery after anesthesia in the surviving rats and the control group. Western blotting was used to detect the expression and dissociation of endothelial nitric oxide synthase (Enos) in pulmonary artery and the nitration level of various proteins in pulmonary artery. The formation of reactive oxygen species (Ros) was detected by DHE-staining in isolated pulmonary arteries. Results in DCS group, 10 rats died after unsafe decompression. The vasodilation ability of pulmonary artery endothelium-dependent in survival rats was significantly decreased. There was no significant difference in the expression of e NOS between the two groups (P 0.05). However, the ratio of e NOS monomer to dimer in DCS group was significantly higher than that in control group (P 0.05). The level of protein tyrosine nitration in pulmonary artery in DCS group was significantly higher than that in control group. The amount of ROS in pulmonary artery in DCS group was significantly higher than that in control group (P 0.05). Conclusion unsafe decompression during simulated submarine escape can lead to the uncoupling of e NOS dimer in pulmonary artery endothelium. The dissociated e NOS monomer could not synthesize no, which affected the endothelium-dependent vasodilation ability. E NOS monomer can promote the synthesis of ONOO, increase the level of protein tyrosine nitration in pulmonary artery, and cause the disorder of cell information regulation. E NOS monomer can also increase the formation of reactive oxygen ion ROS, thus mediating peroxidation damage.
【作者单位】：南方医科大学第三临床医学院;海军总医院干部呼吸内科;海军医学研究所;
【基金】：军队中医药科研专项课题(10ZYZ219)~~
【分类号】：R845.21
【正文快照】： 目前国内外学者普遍认为,不安全减压可导致血管及组织内气泡形成,而减压性血管内气泡形成后是否导致循环障碍与血管功能状态有直接关系[1]。相关研究表明,不管气泡的直径是否大于血管管径(实际上每一个可见气泡的直径都大于微血管管径,至少必定大于毛细血管的管径),气泡的流速

【参考文献】