摘要
目的：探讨胰腺炎大鼠胰腺血流下降的机制和前列腺素E1（PGE1）的治疗作用。方法：向大鼠胰管内注入5％磺酸胆酸钠，制成急性出血坏死型胰腺炎模型。结果：胰头部血流立即下降；胰腺组织中性粒细胞髓过氧化酶（MPO）活性、脂质过氧化物（LPO）水平及毛细血管通透性明显升高；血浆血栓素A2（TXA2）与前列环素（PGI2）比例增加。预先使用PGE1可延缓胰头部血流下降；降低MPO、LPO和毛细血管通透性；抑制血栓素B2，但对6-酮-前列腺素F1a影响较小。结论：胰腺炎初期存在缺血-再灌注过程。胰头部血流下降是TXA2与PGI2平衡失调致血管运动功能紊乱，中性粒细胞（PMN）活化释放氧自由基致血管内皮细胞损伤的结果。PGE1可抑制PMN活化和氧自由基释放，减轻内皮细胞损伤；改善TXA2与PGI2二者平衡，调节血管运动功能，减轻胰腺损伤。
Objective:To investigate the potential mechanism concerning pancreatic blood flow reduction and the protective effects of prostaglandin E1 (PGE1) on rats with acute necrotizing pancreatitis.Methods: A rat model of acute necrotizing pancreatitis (ANP) was produced by retrggrade infusion of5% sodium taurocholate into the pancreatic duct. Results: Following the induction of ANP, it showedthat blood flow in'pancreatic head (BFPH) was decreased,myeloperoxidase (MPO) activity and lipoperoxides (LPO) levels in pancreas and pancreatic capillary permeability (PCP) were significantly increased. Concomitantly,thromboxane A2 (TXA2) to prostaglandin I2 (PGI2) ratios were also elevated.However, pretreatment with PGE, resulted in obvious increase in BFPH and decrease in PCP,MPO,LPO as well as thromboxane B, levels,without marked influence on plasma 6 - keto - prostaglandin F1a.Conclusions: Ischemia - reper fusion occurs during early phase of ANP. Reduction in BFPH appears to beassociated with the imbalance of TXA2 to PGI2,subsequently leading to disorder of vasomotor functionand damage of vascular endothelium due to activation of polymorphonuclear cells (PMN) and release ofoxygen free radicals (OFR). Treatment with PGE1 can markedly increase BFPH by inhibiting activationof PMN and release of OFR,reducing endothelium damage,and improving TXA2 to PGI2 ratio as well asvasomotor function.
出处
《中国危重病急救医学》
CAS
CSCD
1998年第3期154-157,共4页
Chinese Critical Care Medicine
关键词
胰腺炎
胰腺血流
前列腺素
治疗
pancreatitis
pancreatic blood flow
prostaglandin
