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作 者:金常娥[1] 吴迪[1] 肖露[1] 傅应云[1] 许兰[1] JIN Chang-e WU Di XIAO lu FU Yin-yun XU Lan(Department of Respiratory and Critical Care Medicine, The Second Chinical Medical College of Jinan University, People's Hospital of Shenzhen, Shenzhen 518020, China)
机构地区:[1]暨南大学第二临床医学院,深圳市人民医院呼吸与危重症医学科,深圳518020
出 处:《微循环学杂志》2017年第2期13-16,共4页Chinese Journal of Microcirculation
基 金:广东省深圳市卫生计生系统科研项目(201501002)
摘 要:目的:探讨脂联素(gAd)影响肺动脉内皮依赖性舒张反应,参与调控肺动脉高压(PAH)的作用。方法:选择36例肺动脉高压(PAH)患者(PAH患者组)和15例体检健康人群(健康对照组),应用ELISA检测两组血浆gAd水平。分离存在PAH和无PAH肺病患者(PAH组和对照组,每组各5例)的三级肺小动脉制成血管环,采用器官浴槽技术先观察比较经去甲肾上腺素(PE)诱导收缩的两组血管环在不同浓度乙酰胆碱作用后的舒张反应;再观察PAH组血管环经gAd干预后在不同浓度乙酰胆碱作用后的舒张效应以及一氧化氮合酶抑制剂(LNAME)对这种效应的影响。结果:PAH患者组血浆gAd水平显著低于健康对照组(P<0.01)。与对照组肺血管环比较,PAH组PE收缩肺动脉环对乙酰胆碱诱导的舒张功能减弱(P<0.05)。与PAH组肺动脉环比较,PAH+gAd组肺动脉环对不同浓度乙酰胆碱诱导的血管舒张功能增强(P<0.01);而L-NAME对这种效应有降低作用(P<0.01)。结论:gAd可诱导肺动脉内皮细胞产生和分泌一氧化氮,促进肺动脉内皮依赖性舒张反应,从而减轻PAH。Objective: To investigate the effect of adiponectin(gAd) on pulmonary artery hypertension (PAH) by regulating endothelium-dependent relaxation. Method: ELISA method was used to assess the level of gAd in plasma of 36 PAH patients (PAH group) and 15 healthy people(control group). After isolating the rings of pulmonary arteriole of patients suffering from lung disease with or without PAH(5 cases), the effects of different concentrations of acetylcholine (ACh) on the relaxation of twogroups of vascular rings induced by norepinephrine (PE) were observed and compared by organ-bath technique. The effects of different concentrations of acetylcholine on the relaxation of vascular rings after gAd intervention in patients with PAH were also observed, and the effects of nitric oxide synthase inhibitor (L-NAME) were observed. Results: The plasma gad in PAH group was significantly lower than that in the control group (P〈0.01). Compared with control group, the diastolic function of PE-contracting pulmonary artery ring reduced induced by acetylcholine in PAH group (P〈0.05). Compared with the PAH pulmonary artery ring, the pulmonary artery ring induced by different concentrations of acetylcholine was enhanced by PAH+gAd intervention (P〈0.01) , and the effect of L-NAME was decreased (P〈0.01) . Conclusion: gAd increases endothelium-dependent relaxation of pulmonary artery by inducing the production of nitric oxide, and finally decreases PAH.
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