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为探讨磷脂酶Ａ２（ＰＬＡ２）及其抑制剂溴苯酰基溴化物（ＢＰＢ）在急性坏死性胰腺炎（ＡＮＰ）中的作用机理，采用切开十二指肠行胆胰管插管注入牛磺胆酸钠的方法诱导大鼠ＡＮＰ，检测胰腺微循环血流量变化、血ＰＬＡ２、血小板激活因子（ＰＡＦ）和血栓素Ｂ２（ＴＸＢ２）水平。进行基于光镜观察的组织学评分和腺泡细胞的超微病理检查。结果显示：急性胰腺炎（ＡＰ）组在诱导后胰腺血流立即剧烈下降，此后的３小时内轻度回升，３小时后持续下降至实验结束。随着病理改变持续加重，ＡＰ组血ＰＬＡ２，ＰＡＦ和ＴＸＢ２水平持续升高。超微结构所见以粗面内质网扩张、酶原颗粒增加为特征。ＢＰＢ治疗组的胰腺血流下降轻于ＡＰ组，与ＡＰ组相比较，其组织学评分表示的病理损害显著减轻，腺泡细胞粗面内质网扩张较轻，酶原颗粒较少。ＢＰＢ组的血ＰＬＡ２，ＰＡＦ和ＴＸＢ２水平显著低于ＡＰ组。结果表明：ＰＬＡ２在ＡＮＰ的发病中起重要作用。应用ＰＬＡ２抑制剂可能是治疗ＡＮＰ的一个有效的新方法。
To investigate the mechanism of phospholipase A2 (PLA2) and its inhibitor bromophenacylbromide (BPB) in acute necrotizing pancreatitis (ANP), we used the incision of duodenum and bile duct for the injection of taurine Sodium cholate method was used to induce ANP in rats. The changes of blood flow in pancreas, PLA2, PAF and TXB2 were measured. Histological scoring based on light microscopy and ultrastructural examination of acinar cells were performed. The results showed that in the acute pancreatitis (AP) group, the blood flow of the pancreas decreased sharply immediately after induction, and then rebounded slightly within 3 hours after the induction, and continued to drop down to the end of the experiment after 3 hours. With the pathological changes continue to aggravate, AP2 levels of PLA2, PAF and TXB2 levels continued to rise. The ultrastructure is characterized by an enlargement of the rough endoplasmic reticulum and an increase of zymogen particles. Compared with AP group, BPH treated group showed less decrease of pancreatic blood flow than that of AP group. Histopathological score of pathological damage was significantly reduced in BPB treated group. The blood levels of PLA2, PAF and TXB2 in BPB group were significantly lower than those in AP group. The results showed that: PLA2 play an important role in the pathogenesis of ANP. The use of PLA2 inhibitors may be an effective new method for the treatment of ANP.