急性重症胰腺炎血液滤过治疗的机制

Mechanism of hemofiltration in treatment of severe acute pancreatitis

目的:探讨血液滤过减轻急性重症胰腺炎(SAP)全身炎症反应的机制. 方法:逆行性胰管注射50 g/L牛黄胆酸钠/自身胆汁制备犬SAP动物模型,2 h后实施血液滤过2 h,并设立对照组(制模后仅给予深静脉穿刺插管而不血液滤过).记录不同时间段心率,12 h处死动物后通过病理学评分评价肺、肝脏和胰腺组织损伤情况,Westen blotting法检测肺和肝脏组织核转录因子NF-κB的核移位及RT-PCR检测肿瘤坏死因子TNF-αmRNA表达,通过比较血滤组和对照组脏器组织炎性激活和损伤的情况,分析血液滤过的作用机制. 结果:血滤前心率两组之间无显著差异,血滤后各时间点均为对照细显著高于血滤组.病理学评分显示血滤减轻肺脏的损伤,而对肝脏和胰腺损伤作用不明显.NF-κB核移位和TNF-αmRNA表达均为血滤组低于对照组. 结论:血液滤过减轻肺、肝脏等远离病灶器官的炎症激活和损伤,这一作用可能同血液中致炎因子的滤过清除有关.

AIM: To study the mechanism of hemofiltration in the reduction of systemic inflammatory response in severe acute pancreatitis (SAP). METHODS: A mixture composed of sodium taurocholate (50 g/L) and bile was antidromicly injected into pancreatic duct of dogs to establish SAP model. Two hours later, hemofiltration was performed (last 2 h). Heart rate, as well as the acute injury scores of lung, liver and pancreas were compared between model and test groups. Nuclear translocation of nuclear factor-κB (NF-κB) was detected by Western blotting, and TNF-α mRNA expression was determined by reverse transcription-polymerase chain reaction. Then the therapeutic mechanism of hemofiltration in SAP was analyzed. RESULTS: Significant decrease of heart rates was observed 8 and 12 h after the hemofiltration (P= 0.0 181<0.05, P= 0.0 141<0.05 respectively). Hemofiltration resulted in reduction of pulmonary pathological score (1±0.63 vs 2.83±0.75, P=0.001<0.01), but did not affect hepatic and pancreatic ones. NF-κB nuclear translocation and TNF-α expression were inhibited by hemofiltration both in lung and in liver. CONCLUSION: Hemofiltration ameliorates pulmonary and hepatic inflammatory response induced by SAP. This may relate to removal of the over-produced pro-inflammatory cytokines from circulation.