肠缺血再灌注时肺泡Ⅱ型上皮细胞凋亡与肺损伤

Apoptosis of alveolar typeⅡepithelial cells in lung injury after intestinal ischemia-reperfusion

目的 观察肠缺血再灌注中肺损伤与肺泡Ⅱ型上皮细胞凋亡的关系及其可能的发生机制。方法 Wistar大鼠，肠系膜上动脉夹闭后松夹造成肠缺血再灌注。不同时间点活杀动物，测肺通透指数、肺泡灌洗液（BALF）和血浆中NO、IL-2含量，分离肺泡Ⅱ型上皮细胞，观察凋亡率。结果与结论 肠缺血再灌注可能引起肺损伤；肠缺血再灌注后肺泡Ⅱ型上皮细胞凋亡率上升，再灌注30 min 达高峰；缺血再灌注后血、BALF中NO、IL-2增加；肺泡Ⅱ型上皮细胞凋亡率与肺通透指数显著相关，BALF中IL-2水平与肺通透指数、肺泡Ⅱ型上皮细胞凋亡率显著相关。

Objective To investigate the role of apoptosis of alveolar type II epithelial cells in lung injury after intestinal ischemia-reperfusion and the mechanism. Methods Superior mesenteric artery in Wistar rat was occluded and declamped to produce intestinal ischemia-reperfusion. All of the animals were killed at different time points, and the alveolar leak index, nitric oxide(NO) and interlukin-2(IL-2) concentrations in serum and bronchoalveolar lavage fluid (BALF) were determined. Alveolar type II epithelial cells were isolated and apoptosis rate was determined. Results and conclusions It was found that intestinal ischemia-reperfusion might result in lung injury: apoptosis rate of alveolar type II epithelial cells increased, peaked at 30 min of reperfusion; NO and IL-2 concentrations in serum and BALF increased after intestinal ischemia-reperfusion. Apoptosis rate of alveolar type II epithelial cells is significantly positively related to alveolar lung leak index, and the concentration of IL-2 in BALF to apoptosis rate and alveolar leak index.