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研究兔体外循环中肺的缺血再灌注损伤并探讨其可能机制。采用兔体外循环模型 ,测定肺组织的丙二醛 (MDA) ,髓过氧化物酶 (MPO) ,一氧化氮 (NO)含量、肺血管通透性 (EB值 )及肺组织湿干比 (W /D值 )。CPB组肺组织MDA含量 (139 4± 17.0 )mmol/ g明显高于对照组 (2 7.6± 1.8)mmol/ g ,P <0 .0 1;MPO含量 (9.4± 0 .6 )u/ g明显高于对照组 (1.9± 0 .7)u/ g ,P <0 .0 1;NO含量 (8.4± 3.8) μmol/ g明显低于对照组(2 0 .9± 1.7) μmol/ g ,P <0 .0 1;W /D值 (8.5± 2 .1)明显高于对照组 (4 .5± 0 .9)P <0 .0 1;EB值 (3.2 33±0 .0 7)明显高于对照组 (1.394± 0 .0 6 ) ,P <0 .0 1。动物实验提示CPB中肺的缺血再灌注是肺损伤的重要原因 ,内源性NO减少是肺损伤的重要环节
To study the pulmonary ischemia-reperfusion injury during cardiopulmonary bypass and to explore its possible mechanism. The model of pulmonary artery circulation was used to measure the contents of malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO), pulmonary vascular permeability (EB) W / D value). The content of MDA in the lung tissue of CPB group was significantly higher than that of the control group (139.4 ± 17.0 mmol / g, P <0.01; MPO content, 9.4 ± 0.6, u / g (1.9 ± 0.7) u / g, P <0.01; NO content (8.4 ± 3.8) μmol / g was significantly lower than that of the control group (20.9 ± 1.7) μmol / g, P <0. 01; W / D value (8.5 ± 2.1) was significantly higher than that of the control group (4.5 ± 0.9) P <0.01; EB value was significantly higher than that of the control group (3.2 33 ± 0. 0 7) Higher than the control group (1.394 ± 0.06), P <0.01. Animal experiments suggest that pulmonary ischemia-reperfusion in CPB is an important cause of lung injury, endogenous NO reduction is an important part of lung injury