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目的研究模拟失重对肺动脉反应性的影响及其机制。方法采用-30°尾悬吊14d大鼠失重模型模拟微重力生理效应,利用离体灌流技术测量对照组和尾悬吊14d组大鼠肺动脉环对苯肾上腺素(PE)、氯化钾(KCl)和乙酰胆碱(Ach)等血管活性物质的反应性及Nω-硝基-L-精氨酸甲酯(L-NAME)对肺动脉收缩反应的影响,免疫印迹分析两组肺动脉内皮型一氧化氮合酶(eNOS)的表达。结果与对照组相比,尾悬吊组对PE和KCl的收缩反应显著下降,对Ach的舒张反应明显增强;L-NAME处理后使尾悬吊组对PE的收缩反应恢复;尾悬吊组大鼠肺动脉组织eNOS表达显著高于对照组。结论模拟失重后肺动脉收缩反应下降,舒张反应增强,肺动脉内皮细胞eNOS表达增加以致舒张产物NO增加是肺动脉收缩反应性下降的主要原因。
Objective To study the effects of simulated weightlessness on pulmonary arterial reactivity and its mechanism. Methods The weightlessness model of -30 ° tail-suspended rats was used to simulate the effects of microgravity. The effects of pulmonary artery rings of rats in the control group and the tail-suspended group on the pulmonary arterial pressure (PE), potassium chloride (KCl ) And acetylcholine (Ach), and the effect of Nω-nitro-L-arginine methyl ester (L-NAME) on pulmonary artery contractile responses. Immunohistochemistry was used to detect the pulmonary arterial endothelial nitric oxide Enzyme (eNOS) expression. Results Compared with the control group, the contractile response of PE and KCl in the tail suspension group was significantly decreased and the relaxation response to Ach was significantly enhanced. After L-NAME treatment, the contractile response of the tail suspension group to PE was restored. The tail suspension group Pulmonary artery tissue eNOS expression was significantly higher than the control group. Conclusion Pulmonary artery contractile response decreased, diastolic response increased, and eNOS expression in pulmonary artery endothelial cells increased after simulated weightlessness, leading to the decrease of pulmonary artery contractile response.