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作 者:张清友[1] 杜军保[1] 张春雨[1] 闫辉[1] 唐朝枢[2]
机构地区:[1]北京大学第一医院儿科,北京100034 [2]北京大学第一医院心血管病研究所,北京100034
出 处:《实用儿科临床杂志》2003年第11期865-867,共3页Journal of Applied Clinical Pediatrics
基 金:教育部博士学科点专项基金(项目编号 :2 0 0 2 0 0 0 10 63 );国家重大基础研究发展规划(973 ) (项目编号:G2 0 0 0 0 5 690 5);国家自然科学基金(项目编号 :3 0 2 713 73 )
摘 要:目的 探讨内源性一氧化氮 (NO)对低氧性肺动脉高压 (PH)大鼠肺动脉硫化氢 (H2 S) /胱硫醚γ 裂解酶 (CSE)体系的调节作用。方法 将 19只大鼠随机分为 3组 :低氧组 ( 7只 )、低氧 +L NAME组 (予NOS抑制剂Nω 硝基 L 精氨酸甲酯处理低氧组 ) ( 6只 )和对照组 ( 6只 )。低氧 2 1d后 ,分别测定肺动脉平均压 ,检测右心室 /左心室 +室间隔 (RV/LV +SP)比值 ,测定肺组织匀浆NO含量、血浆H2 S含量及肺组织匀浆CSE活性变化。结果 低氧 2 1d大鼠肺动脉平均压力和RV/LV +SP明显增高 ,同时肺组织中NO和血浆H2 S含量及肺组织CSE活性亦明显下降 (P均 <0 .0 1) ;而低氧 +L NAME组 ,伴随NO含量的下降 ,肺动脉平均压亦显著上升 (P <0 .0 5 ) ,同时血浆H2 S含量及肺组织CSE活性较低氧组显著上升 (P均 <0 .0 5 )。结论 内源性NO对肺动脉H2 S/CSE系统在低氧性PH大鼠中呈抑制作用 ,这一过程参与低氧性PH形成的调控机制。Objective To explore the impact of endogenous nitric oxide(NO) on the H 2S/cystahionine γ lyase(CSE) system in pulmonary artery of hypoxic rats.Methods Ninteen rats were randomly divided into 3 groups:hypoxic group ( n =7), hypoxic + L-NAME group ( n =6) and control group ( n =6). After 21 days, mean pulmonary artery pressure (mPAP) of each rat was evaluated and the ratio of right ventricular mass to left ventricular plus septum mass was detected. Meanwhile, the production of NO in pulmonary tissue, the plasma concentration of H 2S and the activity of CSE in pulmonary tissue were detected.Results Mean PAP and RV/LV+SP significantly increased in hypoxic rats as compared with those of normal controls ( P <0.01). Meanwhile, compared with controls, the production of NO in pulmonary tissue, the plasma concentration of H 2S and the activity of CSE in pulmonary tissue markedly decreased in hypoxic rats( P <0.01, respectively). However, mPAP and RV/LV+SP were significantly increased in hypoxic + L-NAME groups as compared with hypoxic groups( P <0.05), at the same time, the production of NO in pulmonary tissue was markedly decreased ( P < 0.01 , respectively). However, the plasma concentration of H 2S and the activity of CSE in pulmonary tissue in hypoxic + L-NAME group increased significantly as compared with those of hypoxic group( P <0.05).Conclusion The endogenous nitric oxide might inhibit H 2S production in pulmonary artery of hypoxic rats.
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