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目的测定大白鼠肠道缺血再灌注损伤后肺表面活性物质（ＰＳ）的浓度及活力，结合肺组织病理改变，探讨急性肺损伤的病理机制。方法健康雄性ＳＤ大白鼠随机分三组：Ａ组（对照）；Ｂ组（肠缺血６０分钟）；Ｃ组（肠缺血６０分钟再灌注１２０分钟）。右肺灌洗后，测灌洗液中总蛋白（ＴＰ）、总磷脂（ＴＰＬ）、饱和磷脂（ＤＳＰＣ）浓度；测左肺上叶干／湿比值；左肺下叶病理检查。结果１、肠道缺血再灌注后肺泡灌洗液中蛋白质含量显著升高（Ａ组与Ｃ组比较Ｐ＜０．０１）；再灌注后总磷脂含量明显低于对照组（Ｐ＜０．０１）。２、肺干／湿比值：缺血组较对照组明显降低Ｐ＜０．０５；再灌注组较对照组降低更为显著Ｐ＜０．０１。３、病理检查：Ｂ组：肺组织内毛细血管充血，间质增宽，水肿，炎症细胞渗出。Ｃ组：肺组织内毛细血管充血，间质增宽，水肿，炎症细胞渗出，部分肺泡不张，肺泡水肿，肺出血。结论肠道缺血再灌注可引起急性肺充血、水肿肺泡不张和肺出血等损伤；在急性肺损伤中，肺表面活性物质的含量明显降低及活力的明显减弱可能为肺部病理改变的原因。
Objective To determine the concentration and viability of pulmonary surfactant (PS) after intestinal ischemia / reperfusion injury in rats and to explore the pathological mechanism of acute lung injury in combination with pathological changes of lung tissue. Methods Healthy male SD rats were randomly divided into three groups: group A (control); group B (intestinal ischemia 60 minutes); group C (intestinal ischemia 60 minutes and reperfusion 120 minutes). After the right lung lavage, the concentration of total protein (TP), total phospholipid (TPL) and saturated phospholipid (DSPC) in the lavage fluid were measured; the left / right upper lobe dry / wet ratio was measured; The results showed that the content of protein in alveolar lavage fluid after intestinal ischemia-reperfusion was significantly increased (P <0.01 in group A and C), and the content of total phospholipid in reperfusion group was significantly lower than that in control group (P <0. 01). 2. Pulmonary wet / dry ratio: the ischemic group was significantly lower than the control group (P <0.05); the reperfusion group was significantly lower than the control group (P <0.01.3); Pathological examination: Group B: Blood vessel congestion, interstitial broadening, edema, inflammatory cell exudation. Group C: pulmonary capillary congestion, interstitial broadening, edema, inflammatory cell exudation, some alveolar atelectasis, alveolar edema, pulmonary hemorrhage. Conclusions Intestinal ischemia-reperfusion can cause acute pulmonary congestion, edematous alveolar atelectasis and pulmonary hemorrhage. In acute lung injury, the decrease of pulmonary surfactant and the obvious decrease of vitality may be the reason of lung pathological changes .