急性坏死性胰腺炎模型大鼠肠血流量及血清磷脂酶A_2、白介素-1β的变化

Changes of intestinal blood flow, serum phospholipase A_2 and interleukin-1β in rats with acute necrotizing pancreatitis

观察了急性坏死性胰腺炎 (acutenecrotizingpancreatitis ,ANP)时肠组织血流量及炎症介质的变化。实验用 96只SD大鼠 ,随机分成对照组和ANP组 ,以 5 %牛磺胆酸钠胰腺被膜下均匀注射复制ANP模型。采用放射生物微球技术在制模后 0h、2h和 12h分别测定肠组织血流量 ,同时检测血清磷脂酶A2 (PLA2 )活性及白细胞介素 1β(IL 1β)水平 ,并观察肠粘膜病理改变。结果显示 ,ANP组在制模后 2h及 12h肠组织血流量 (0 80± 0 0 7,0 5 0± 0 0 6 )mL (min·g)较对照组 (1 5 6± 0 18,1 6 1± 0 11)mL (min·g)明显减少 (均P <0 0 0 1) ,血清PLA2 活性 (94 2 9± 9 96 ,10 3 71±14 4 0 )U L ,IL 1β水平 (0 78± 0 13,0 83± 0 2 0 ) μg L较对照组 (6 5 2 7± 10 5 2 ,6 6 6 3± 9 81)U L ,(0 32± 0 0 6 ,0 33±0 0 7) μg L明显升高 (均P <0 0 0 1) ,肠粘膜损伤程度较对照组明显加重 (均P <0 0 0 1)。提示ANP早期肠组织血流量减少与炎症介质的升高同时发生 。

To explore the relationship between intestinal ischemia and inflammatory mediators released in rats with acute necrotizing pancreatitis(ANP). A total of 96 rats were randomized as control group and ANP group. The ANP model was induced by injection of 5% sodium taurocholate under the pancreatic capsule. Redioactive biomicrosphere technique was used to measure the intestinal tissue blood flow at 0h, 2h and 12h after the induction of ANP, meanwhile, blood and intestinal tissue samples were taken for observation of phospholipase A 2 (PLA 2), interleukin 1β(IL 1β) level intestinal mucosal pathological changes. Experimental results demonstrated that intestinal blood flow in ANP group (0.80±0.07, 0.50± 0.06)mL/(min·g) was significantly lower than control group (1.56±0.18, 1.61±0.11)mL/(min·g), the PLA 2 activities (94.29±9.96, 103.71±14.40)U/L and IL 1β levels (0.78±0.13, 0.83±0.20)μg/L in SAP group were higher than that of control group (65.27±10.52, 66.63±9.81)U/L, (0.32±0.06, 0.33±0.07) μg/L (all P <0.001 ). Comparing with control group, the intestinal mucosal pathological changes was significantly aggravated(all P <0.001 ) at 2h and 12h after induction of ANP. which suggests that the decrease of intestinal blood flow and the increase of inflammatory mediators develop simultaneously in early phase of ANP, hence both of them are important pathogenic factors of intestinal mucosal injury in ANP.