重症急性胰腺炎对血清胰岛素和胰高血糖素影响的实验研究

Effects of Severe Acute Pancreatitis on the Level of Serum Insulin and Glucagon in Rats

目的研究重症急性胰腺炎对血清胰岛素和胰高血糖素的影响。方法应用3.5%牛磺胆酸钠逆行注入大鼠胰胆管,制作大鼠重症急性胰腺炎6h、24h、48h、72h动物模型,对胰腺病理损伤评分;免疫组化方法观察胰腺Bcl-2表达情况;放射免疫分析法测定血清胰岛素、胰高血糖素水平。结果重症急性胰腺炎大鼠造模后,随时间延长胰腺损伤加重,以24h为最;重症急性胰腺炎组大鼠血清胰岛素水平与实验对照组、正常对照组在24h、48h、72h相比明显下降,差异有统计学意义(P<0.05)。重症急性胰腺炎大鼠血清胰高血糖素水平制模后6h、24h、48h、72h与实验对照组、正常对照组相比明显升高,差异有统计学意义(P<0.05)。结论重症急性胰腺炎对胰腺内分泌有较大影响,在重症急性胰腺炎早期内分泌功能损伤的同时,机体可能存在一定的保护机制,Bcl-2可能参与了保护作用。

Objective To study the effects of severe acute pancreatitis on the level of serum insulin and glucagon in rats. Methods SAP model was produced by retrograde injection of 3.5% sodium taurocholate into the cannulated biliopancreatic duct, and rats were sacrificed at 6, 24, 48, 72 h after induction of pancreatitis. The pancreatic tissue specimens were collected to assess the pathological score of exocrine part in terms of tissue damage and Bcl-2 expression was observed with immunohistochemical examination. Prior to sacrifice, blood samples in 6, 24, 48, 72 h were taken from the inferior vena cava to measure serum insulin and glucagons with radioimmunoassay (RIA). Results Tissue damage got worse with time passing and maximized at 24 h after SAP model established. With the development of disorder, the pancreas presented necrosis, hemorrhage and severe leukocytes infiltration. The serum insulin level markedly decreased at 24, 48, 72 h, and the level of glucagon significantly increased at 6, 24, 48, 72 h compared with the experimental control group and normal control group. The differences were significant statistically. Immunohistochemistry examination showed that the Bcl-2 expressed in islets of SAP rats after 6 h, however disappeared after 24 h. Conclusion Severe acute pancreatitis impairs both the pancreatic exocrine and endocrine functions. On the other hand, the Bcl-2 expression in immunohistological examination indicated that there might be a protective mechanism against the endocrine dysfunction in SAP, in which Bcl-2 was involved.