缺血后处理调控炎症介质对心肌缺血再灌注后急性肺损伤的保护作用

Role of Inflammatory Factor During Ischemic Postconditioning on Acute Lung Injury Induced by Myocardial Ischemia-Reperfusion in Rats

目的：探讨缺血后处理对于心肌缺血再灌注所致急性肺损伤的保护作用及其对炎症介质的作用机制。方法：健康雄性大鼠36只,随机均分为如下3组：假手术组（S组）、心肌缺血再灌注组（I/R组）及其心肌缺血后处理组（IPO组）。采用心肌缺血再灌注模型和心肌缺血后处理模型。于再灌注2h后采集颈动脉血样,然后处死大鼠,取肺组织,镜下观察肺组织病理改变,并行病理学损伤评分。检测肺水肿程度、肺血管通透性以检测肺功能改变,检测血清及肺炎症因子TNF-α、IL-1β和IL-10的含量。结果：与S组比较,I/R组肺组织病理学损伤评分升高（P〈0.05）,肺水肿程度增加（P〈0.05）,肺血管通透性增强（P〈0.05）,I/R组炎症因子TNF-α和IL-1β含量显著增高（P〈0.05）,抗炎因子IL-10的含量显著降低（P〈0.05）。心肌缺血后处理后,IPO组较I/R组TNF-α和IL-1β明显降低（P〈0.05）,但仍高于S组（P〈0.05）。IL-10较I/R组显著增高（P〈0.05）。炎症因子TNF-α、IL-1β和IL-10在血清的含量变化与肺组织中表达变化趋势一致。结论：心肌缺血后处理通过调控抗炎/促炎平衡,进而减轻心肌缺血再灌注所致的急性肺损伤。

Objective： To investigate the protective effect of myocardial ischemic postconditioning （IPO） on acute lung injury induced by myocardial ischemia-reperfusion in rats. Methods. A total of 36 healthy male SD rats were randomly divided into 3 groups： sham operation group （S group）, is chemia-reperfusion group （I/R group）,ischemic postconditioning ＋ ischemia-reperfusion group （IPO group）. The rats model of myocardial ischemia-reperfusion and ischemic postconditioning were adopted. Blood samples were collected by carotid artery after 2 h reperfusion,the lung tissue were collected after rats were sacrificed, pulmonary microvascular permeability and assessment of pulmonary edema were detected to evaluate the lung function. Lung tissue sections were taken for light microscopic observation. TNF-α,IL-1β and IL-10 content in the serum and lung were meas- ured. Results：In comparison with that in S group, lung tissue injury in I/R group was more se- vere under light microscope （P〈0.05）. The mean wet/dry weight ratio and permeation index of lung in I/R group were significantly higher than those in S group （P〈0.05）. The expression of TNF-α and IL-1β in I/R group were significantly increaced than those in S group （P〈0. 05）, while the expression of IL-10 in I/R group was decreased than that in S group （P〈0.05）. After myocardial IPO, the degree of lung tissue injury had been reduced as compared with that in I/R group（P〈0.05）, the mean wet/dry weight ratio and permeation index of lung were remarkably lower than those in I/R group （P〈0.05）. The expressions of TNF-α and IL-1β in IPO group were definitely decreased than those in I/R group （P〈0.05）, while the expression of IL-10 was increased （P〈0.05）. The changes of TNF-α, IL-1β and IL-10 in the serum were consistent with those expression in lung tissue. Conclusion. Rhythmic stimulation of ischemic postconditioning attenuates acute lung injury induced by myocardial ischemia-reperfusion. The protective mecha- nism may be related to the regulation of anti-inflammatory/proinflammatory balance.