重症急性胰腺炎时肾功能受损机理的实验研究

Pathogenesis of kidney injury in severe acute pancreatitis rats

目的:探讨重症急性胰腺炎(SAP)时血浆细胞因子、内毒素和血管紧张素(AT)的动态变化及其与肾损伤的关系。方法:将SD大鼠(清洁级)60只随机分为假手术组(n=30)和SAP组(n=30)。采用胰管内逆行注射4%牛黄胆酸钠溶液的方法制作SAP模型。观察胰腺和肾脏的病理改变,动态测定血浆TNF、IL-6、LPS、ATⅡ和BUN、Cr水平。结果:制模后血浆TNF、IL-6、LPS、ATⅡ水平升高,24 h升高明显,48 h达到高峰,72 h仍维持较高水平。结论:SAP早期即有肾功能损害的发生,其中细胞因子、内毒素和肾素/血管紧张素系统的激活参与了肾功能受损的发生发展过程,并随着病情的发展,肾功能受损不断加重。

Objective To explore the relationship between the changes of plasma cytokines, LPS, angiotensin Ⅱ and the renal injury in severe acute pancreatitis （SAP） rats. Methods SD rats were divided randomly into sham operation group（ n = 30 ） and SAP group（ n = 30）. SAP animal model was established in adult male rats by retrograde injection of 4% sodium laurocholate 1 ml/kg in biliopancreatic duct. Morphology of pancreas and kidneys were observed. Plasma levels of TNF, IL - 6, LPS,AT Ⅱ and BUN, Cr were measured at various time points. Results The plasma levels of TNF,IL-6,LPS and AT Ⅱ was increased after SAP induction and there was a significant increase after 24 h, their levels reached a peak at 48 h, and remained at high level at 72 h. Conclusion The levels of TNF,IL-6 ,LPS,AT Ⅱ was increased and the renal function was injured in the early stage of SAP. Cytokines, LPS, and activated renin - angiotensin system might be involved in pathogenesis of kidney injury following SAP. The renal function damage was increased with severity of SAP. There was a close relationship between kidney injury and pancreatitis.