重症急性胰腺炎相关肺损伤危险期的确立

目的 通过对重症急性胰腺炎模型小鼠肺组织含水量、Ⅱ型肺泡上皮细胞的超微结构及数目、活性氧代谢产物的动态演变研究和临床资料的分析,从基础和临床的角度综合确立重症急性胰腺炎相关肺损伤的危险期.方法 ICR清洁级小鼠雨蛙素腹腔内注射50 μg/kg,每小时1次,共7次,于雨蛙素注射结束后腹腔内注射LPS 15 mg/kg来创建重症急性胰腺炎小鼠模型,设定研究点为制模前、制模后6 h、12 h、1 d,4 d、7 d,对肺组织含水量、Ⅱ型肺泡上皮细胞的超微结构和数目以及肺组织活性氧代谢产物进行了动态研究.同时回顾性分析215例来自于浙江大学医学院附属第一医院1998年1月至2006年12月收治在消化内科、胰腺外科和ICU的重症急性胰腺炎患者伴肺损伤患者(纳入标准为PaO2<60 mmHg)肺损伤的时期.样本均数差异采用F检验,P<0.05为差异有统计学意义.结果 重症急性胰腺炎小鼠肺组织含水量以制模后1 d和4 d最严蕈,Ⅱ型肺泡上皮细胞的线粒体和板层小体损伤程度以制模后1 d,4 d最为明显,Ⅱ型肺泡上皮细胞数目下降以制模后1 d最显著,肺组织活性氧代谢产物亦以制模后1 d明显升高,较其他研究点有显著性差异.临床上重症急性胰腺炎患者出现肺损伤的时间为(3.1435±1.0199)d.结论 重症急性胰腺炎相关肺损伤的危险期在重症急性胰腺炎病程的第1天至第4天之间.

Confirmation of the critical period of severe acute pancreatitis-associated lung injury

Objective To define the risk period of acute pancreafifis-associated lung injury (APALI) by aserial study including a dynamic changes in total water content of lung, ultrastructure and number of type Ⅱ alveo-lar epithelial, and reactive oxygen metabolisms (ROMs) of lung tissue in mice with severe acute pancreatits (SAP)and a clinical analysis of APALI patients. Method ICR mice were selected to establish SAP model. The animalsreceived 7 intraperitoneal injections of caerulein (50 μg/kg body weight) at hourly intervals followed by intraperi-toueal injection of lipopolysaccharide (15 mg/kg body weight). The total water content, uhrastrueture and numberof type Ⅱ alveolar epithelial cells, and ROMs of lung tissue were detected before (0 h) and 6 hours, 12 hours,lday, 4 days and 7 days after SAP model establishment, respectively. In addition, 215 patients with APALI (PaO2< 60 mmHg) collected from the First Affiliated Hospital of Zhejiaug University between January 1998 and Decem-ber 2006 were analyzed. Statistical analysis were performed by using F-test. P-values less than 0.05 were regardedas statistically significant. Results The total water content and ultrastructure mitochondria and lamellar bodies intype Ⅱ alveolar epithelial cells of lung in SAP mice were significantly altered at 12 hours after SAP model estab-lishment, and reached maximum at 1 to 4 days later. A decrease in number of type Ⅱ alveolar epithelial cells andincrease in ROMs reached a maximum at 1 day after SAP model establishment. Furthermore, the results of clinicalstudy showed that the lung injury occurred at (3.1435±1.0199) days after SAP. The data were almost consistentwith the resalts from SAP model. Conclusions The risk period of APALI occurres between the 1st day and the4th day during the course of SAP.