【摘要】 目的 :探讨重症急性胰腺炎 (SAP)时炎症介质的动态变化及其与肾损害的关系。方法 :SD大鼠 64只 ,随机分为对照组与SAP组 ,用 5 %牛磺胆酸钠胰腺被膜下均匀注射制成SAP模型 ,术后 0 .5h、2h、6h、12h分别观察血液中炎症介质、BUN、Cr及肾组织学的改变。结果 :与对照组相比 ,SAP组各时相BUN、Cr、TNFα 和IL 1 β均明显增高 ,TXA2 PGI2 比值于术后 2h起明显增高 ,肾组织学改变随时间延长而加重。结论 :SAP早期即发生肾功能损害 ,TNTα、IL 1的异常以及TXA2 与PGI2 的失衡参与了SAP肾损害的发生机制 ,抑制或预防炎症介质的产生可能防治SAP时的肾损害。更多还原

【Abstract】 Objective: To explore the relation between the changes of intlammatory mediators and the renal damage following severe acute pancreatitis(SAP). Methods: A total of 64 rats were randomized into control group and SAP group. The model of SAP was established by uniform injection of 5% Sodium taurocholate solution into pancreatic capsule. Then blood samples and renal tissues were collected at the 0.5h、、2h、6h and 12h after SAP to measure levels of BUN、Cr、TNF α、IL 1、TXA 2/PGI 2 and examine renal histological changes. Results: Plasma levels of BUN、Cr、TNF α、and IL 1 were significantly higher in the SAP group than in the control gronp, and the ratio of TXA 2/PGI 2were significantly higher since 2h after SAP, renal damages were found in SAP group. Meanwhile, they were increased with aggravation of SAP. Conclutions: Renal damage are found in SAP early, TNF α、IL 1 and TXA 2/PGI 2 might be involved in pathogenesis of the renal damage following SAP. Reducing plasma levls of TNF α、IL 1and the ratio of TXA 2/PGI 2 might alleviate renal damage.更多还原