体外循环影响内源性肺表面活性物质的机制

Mechanism of Effect of Cardiopulmonary Bypass on Endogenous Pulmonary Surfactant

探讨体外循环影响内源性肺表面活性物质的机制。方法采用Ｂａｒｔｌｅｔ法、Ｍａｓｏｎ法、Ｌｏｗｒｙ法、抗原抗体斑点杂交法测定１０头实验用小型猪体外循环前后气道吸出物中肺表面活性物质的活性。同步分别用酶联免疫法和硫代巴比妥酸反应法测定肺静脉血肿瘤坏死因子和丙二醛的含量；测定肺组织含水量和进行超微结构观察。结果体外循环后内源性肺表面活性物质的活性明显降低（Ｐ＜０．０１），且这种异常变化与肿瘤坏死因子、丙二醛的含量及肺含水量的明显增加均有显著相关关系（ｒ＝－０．９１、－０．７５、－０．９２，Ｐ＜０．０１）。同时发现体外循环后肺泡Ⅱ型上皮细胞受损，肺泡—毛细血管膜通透性增高，肺泡腔内液体积聚，蛋白质渗入明显。结论体外循环时肺的缺血—再灌注损伤导致内源性肺表面活性物质合成不足；过度稀释，消耗增加；活性受到抑制。

Purpose To study the mechanism of the effect of cardiopulmonary bypass on endogenous pulmonary surfactany(PS). Methods In 10 piglets undergoing cardiopulmonary bypass(CPB),saturated phosphatidylcholine (SatPC),total phospholipids(TPL),total protein(TP) and surfactant protein A (SP-A) in sequential airway aspirates before and after operation were determined.At the same time,the concentration of plasma molondealdehyde(MDA) and tumor necrosis factor α(TNFα)were simultaneously analysed with ELISA and Satrh TBA methods respectively .The histological examination of the lungs under electron microscope was performed as well. Results The values of SatPC/TPL,SatPC/TP and SP-A/TP were decreased significantly( P < 0.01 )after CPB.These abnormal changes of endogenous PS were closely correlated to the increase of MDA,TNFα and lung water( P< 0.01).Histological examination of the lungs under electron microscope confirmed that after CPB type Ⅱ pneumocytes were damaged,and the permeability of alveoli capillary membrane was increased.In addition,fluid was accumulatied in the alveoli and protein diffusion into the alveoli was significant.Conclusions [WT10.BZ〗The pulmonary ischemia reperfusion injury resulted in insufficient synthesis of PS and limitation of its activity.