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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 levels and expression of endothelin - 1 (ET - 1), endothelial nitric oxide synthase (eNOS) and malondialdehyde (MDA) in the hemorrhagic lung tissue of neonatal rats, The relationship between people. Methods Fifty new Wistar rats were randomly divided into normal control group (n = 10) and experimental group (n = 40). After tracheal intubation, the control group was given 30 μl of normal saline, and the experimental group was dripped with exogenous ET 130 μl at a concentration of 4 × 10-6 mol / L. The animals were sacrificed 3 hours after the dropping of the drug, and the gross pathology of lung tissue, changes of HE staining, enET 1, eNOS immunohistochemistry and MDA content in lung tissue were observed. Immunohistochemical staining, the cells were brown to yellow positive. Results Exogenous ET - 1 tracheal instillation, can cause different degrees of PH. EnET 1 in experimental group was significantly higher than that in control group (P <0.05), diffuse PH was higher than point-like PH (P <0 05), while eNOS was significantly higher than that in control group Lower than the control group (P <0 05), diffuse PH was lower than the point PH (P <0 05). The content of MDA in the experimental group was significantly higher than that in the control group (P <0.05). The diffuse PH was higher than the point-like and focal PH (P <0 05). Conclusion Endotracheal ET - 1 tracheal instillation can lead to acute hypoxia and stimulate abnormal subenvironmental secretion of enET 1 in pulmonary vascular endothelial cells. enET 1 inhibits eNOS activity through an autocrine pathway and induces the massive production of oxygen free radicals, eventually damaging the pulmonary vascular endothelium causing PH.