胰蛋白酶所致大鼠急性肺损伤模型的建立与评估

The establishment and evaluation of the rat model in acute lung injury caused by trypsin

目的 研究经大鼠尾静脉持续注射胰蛋白酶的方法建立胰蛋白酶诱导的急性肺损伤的动物模型,并对模型进行评估.方法 通过大鼠尾静脉连续注射胰蛋白酶制备胰蛋白酶诱导的大鼠肺损伤模型,分别于造模成功后3、6、12、24h后处死,行肺组织病理学观察,结合外周血中性粒细胞计数,动脉血氧分压（PaO2）、二氧化碳分压（PaCO2）及大鼠肺组织湿/干质量比（W/D）对模型进行评估.结果 HE染色结果显示,对照组大鼠肺组织无明显病理改变,模型组肺组织肺泡和肺间隔水肿、增宽并有大量的炎性细胞浸润.与对照组相比,模型组外周血中性粒细胞计数、PaCO2、W/D显著增加,PaO2显著降低,其差异均有统计学意义（P＜0.01）;模型组不同时间点外周血中性粒细胞计数、PaCO2、W/D、Pa02比较差异有统计学意义（P＜0.01）.结论 胰蛋白酶诱导的大鼠急性肺损伤模型可以成功模拟重症急性胰腺炎时胰蛋白酶大量释放入血所造成的肺损伤.

Objective To investigate the animal model of acute lung injury （ALI） induced by caudal vein injection of trypsin in rats and to evaluate the model.Methods The model of lung injury was established by caudal vein injection of trypsin in rats.The rats were killed at the time point of 3 h,6 h,12 h,24 h,and 24 h and then the pathological changes of structure of lungs,peripheral blood neutrophil count,arterial blood gas analysis and lung wet/dry （W/D） weight ratio in rats were measured and observed.Results The results of hematoxylin eosin （HE） staining showed that there was no obvious pathological changes in lung tissues of the control group,while alveolar and pulmonary septal edema,thickening,and a large number of inflammatory cells infiltration in the lung tissues of the model group.Compared to the control group,the peripheral blood neutrophil counts,W/D and PaCO2 were significantly increased,PaO2 was significantly decreased （P 〈0.01）.There was significant differences in the number of peripheral blood neutrophils,PaCO2,W/D and PaO2 between the model groups （P 〈 0.01）.Conclusions The rat model of ALI induced by trypsin can successfully simulate the lung damage caused by the release of a large number of trypsin when severe acute pancreatitis occurred.