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新生鼠肺出血时肺组织中内皮素-1、一氧化氮合成酶及丙二醛的水平与表达 被引量:8

The level and expression of endogenous endothelin-1,endothelial nitric oxide synthase and malondialdehyde induced by exogenous endothelin-1 in the hemorrhagic lung tissue of newborn rats
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摘要 目的 研究新生鼠出血肺组织中内源性内皮素 1(enET - 1) ,内皮型一氧化氮合成酶 (eNOS)及丙二醛 (MDA)的水平与表达 ,探讨肺出血 (PH)时三者之间的关系。方法  5 0只新生Wistar大鼠随机分正常对照组 10只 ,实验组 4 0只。气管插管后 ,对照组滴入生理盐水 30 μl,实验组滴入浓度为 4× 10 - 6mol/L的外源性ET 130 μl。滴药 3h后处死动物 ,观察肺组织大体病理、HE染片改变、enET 1、eNOS免疫组化及肺组织MDA含量。免疫组化染片中 ,细胞显棕黄色至黄色为阳性。结果 外源性ET - 1气管内滴入 ,可引起不同程度PH。比较免疫组化阳性表达率和阳性反应强度 ,实验组enET 1明显高于对照组 (P <0 0 5 ) ,其中弥漫性PH高于点状PH (P <0 0 5 ) ;而eNOS则明显低于对照组 (P <0 0 5 ) ,其中弥漫性PH又低于点状PH (P <0 0 5 )。实验组MDA含量明显高于对照组 (P <0 0 5 ) ,其中弥漫性PH高于点状及局灶性PH (P <0 0 5 )。结论 外源性ET - 1气管内滴入 ,可导致急性缺氧 ,刺激肺血管内皮细胞中enET 1异常亚持续分泌。enET 1通过自分泌途径 ,抑制eNOS活性 ,并诱导氧自由基大量生成 ,最终损害肺血管内皮细胞而致PH。 Objective To study the level and expression of endogenous endothelin-1(enET-1), endothelial nitric oxide synthase (eNOS)and malondialdehyde (MDA)induced by exogenous endothelin-1(exET-) in the hemorrhagic lung tissue of newborn rats, and to explore their relationship in pulomary hemorrhage (PH).Methods 50 Wistar newborn rats were randomly assigned into control group and experiment group(n=40). 30 μl of normal saline in control group and of 4×10 -6 mol/L concentration exET-1 in experiment group were infused through endotracheal tube.3 h after infusion, the rats were killed.The gross anatomy, HE stain , immunohistochemistry of ET-1 and eNOS,and variation of MDA in pulmonary tissue were observed in each group.Results Administering exET-1 through tracheal caused different degree of PH.The rate of positive expression and the intensity of positive reaction, enET-1 were higher in experiment group than in those control group(P<0.05 ).These level were lower in extensive PH than in spotted PH(P<0.05 ).MDA were higher than in control group(P<0.05)and the level were higher in extensive PH than in local PH and spotted PH(P<0.05).Conclusion exET-1 infusion through tracheal can cause acute hypoxia,which can stimulate enET-1 release abnormally and persistently by pulmonary vascular endothelial cells.Ativity of eNOS is inhibited and oxygen free radical is produced mostly by autocrine pathway of ET-1and PH at last.
出处 《中华急诊医学杂志》 CAS CSCD 2004年第7期453-456,共4页 Chinese Journal of Emergency Medicine
基金 广州市计划委员会资助项目 [穗科技 ( 1998) 11号 ]
关键词 新生鼠 肺出血 肺组织 内皮素-1 一氧化氮合成酶 丙二醛 Newborn rat ET-1 eNOS MDA Pulmonary hemorrhage
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