控制性肺膨胀对兔外源性肺损伤的疗效及其机制探讨

摘要

目的：探讨控制性肺膨胀对外源性急性肺损伤动物模型肺保护作用及其机制。方法应用静脉注射油酸成功复制外源性急性肺损伤模型，免疫组织化学方法检测肺组织IL⁃10和IL⁃6蛋白表达；用ELISA双抗夹心法检测血清中IL⁃10和IL⁃6含量；Western blot检测肺组织和肺泡灌洗液中SP⁃A蛋白表达；逆转录PCR测定肺组织中ICAM⁃1 mRNA和SP⁃A mRNA表达；流式细胞仪定量分析肺组织细胞凋亡。结果35 cmH2O压力维持20 s的肺复张方法能有效提高PaO2和PaO2/FiO2，降低PaCO2，改善氧合和肺顺应性，对肺外源性急性肺损伤的复张效果良好；与对照组比较，控制性肺膨胀治疗组肺组织和血清IL⁃10及IL⁃6含量明显增高（P<0.05），肺组织和肺泡灌洗液SP⁃A表达水平显著减少（P<0.05）；流式细胞仪检测结果显示，实验组细胞凋亡率明显高于对照组（P<0.05）。结论控制性肺膨胀可通过抑制凋亡，减轻急性肺损伤时的炎性反应，降低肺水肿程度，减少肺组织SP⁃A降解，促进肺泡SP⁃A合成与分泌，对外源性急性肺损伤的保护作用较好。%Objective To evaluate the lung protective effect of sustained inflation(SI)and its mechanism for exogenous acute lung injury(ALI) animal models. Methods Exogenous acute lung injury animal models were replicated using intravenous injection of oleic acid. Immunohistochemis⁃try and double antibody sandwich ELISA were carried out to detect IL⁃10 and IL⁃6 protein levels in lung tissues and serum. Western blot was used to detect the expression level of SP⁃A in lung tissue and bronchoalveolar lavage fluid(BALF). The expression of ICAM⁃1 and SP⁃A mRNA in lung tis⁃sue was measured by reverse transcription PCR. The apoptosis of lung tissue cells was detected by flow cytometry. Results The maintenance of 20 s lung recruitment method of 35 cmH2O pressure could improve PaO2 and PaO2/FiO2,reduce PaCO2,and improve oxygenation and pulmonary com⁃pliance. The re⁃expansion effect of sustained inflation for exogenous acute lung injury was good. The IL⁃10 and IL⁃6 levels in lung tissue and serum for SI group were significantly higher than those of the control group(P<0.05). The SP⁃A expression level of lung tissue and BALF in SI group was significantly reduced compared with the control group(P<0.05). Flow cytometry analysis showed that the apoptosis rate of SI group was significant⁃ly higher than that of the control group(P<0.05). Conclusion Sustained inflation played an important role in lung protection against exogenous ALI through inhibition of apoptosis,lightening of inflammatory response,reduction of pulmonary edema and SP⁃A degradation in lung tissue,as well as promotion of SP⁃A synthesis and secretion in pulmonary alveolus.