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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 mechanism of pancreatic blood flow decline in rats with pancreatitis and prostaglandin E1 (PGE1) therapeutic effect. Methods: 5% sulfonate sodium cholate was injected into the pancreatic duct of rats to make acute hemorrhagic necrosis pancreatitis model. Results: The blood flow of pancreas decreased immediately. The activities of MPO, LPO and capillary permeability of pancreas were significantly increased. The levels of plasma TXA2 ) And prostacyclin (PGI2) increased. Pretreatment with PGE1 slowed the decline of blood flow in the pancreas head; decreased MPO, LPO and capillary permeability; inhibited thromboxane B2 but had less effect on 6-keto-prostaglandin F1a. Conclusion: There is ischemia-reperfusion process in the early stage of pancreatitis. Decreased blood flow in the head of pancreas is a result of vascular motor dysfunction induced by imbalance of TXA2 and PGI2, and activation and release of oxygen free radicals by neutrophils (PMNs). PGE1 can inhibit PMN activation and oxygen free radical release, reduce endothelial cell damage; improve the balance of TXA2 and PGI2 both regulate vascular motor function and reduce pancreatic injury.