急性胰腺炎的发病是各种病因引起胰腺腺细胞的损害,胰腺和腺细胞内胰酶活化并逸脱到胰腺间质而导致胰腺自身消化。引起胰腺自身消化的始动因素是胰蛋白酶,少量胰蛋白酶原活化为胰蛋白酶,它可使胰蛋白酶原、糜蛋白酶原、弹力纤维酶原、羧肽酶原、血管舒缓素原、磷脂酶原A等胰酶相继活化,而损害胰腺组织。活化胰酶逸脱到血中可引起肾功不全、呼吸衰竭、肝功能障碍等多脏器损害,使病情恶化和发生休克,DIC等。因而抗胰酶疗法日益引起人们的重视,有人认为是治疗急性胰腺炎的内科疗法的中心。一、抗胰酶疗法的作用原理:胰酶活化后的破坏作用主要是通过胰蛋白酶和胰脂肪酶的消化作用产生的。弹力纤维酶原活化为弹力纤维酶破坏血管引起胰腺出血。磷脂酶原A活化为磷脂酶A使卵磷脂转变为溶血卵磷脂,溶血卵磷脂破坏细胞膜引起胰腺实质坏死及脂肪坏死。激肽原激活为各种激肽,特别是缓激肽,可引起内脏血管扩张、通透性增强、血容量减少 The incidence of acute pancreatitis is caused by various causes of damage to pancreatic gland cells, pancreatic and glandular pancreatic enzyme activation and escape to the pancreatic stroma and cause the pancreas to digest itself. The initial cause of pancreatic digestion is trypsin, a small amount of trypsin activation of trypsin, it can make trypsinogen, chymotrypsinogen, elastase, carboxypeptidase, kallikrein, phospholipase A and other pancreatic enzymes have been activated, while damage to pancreatic tissue. Activation of trypsin escape to the blood can cause renal insufficiency, respiratory failure, liver damage and other multiple organ damage, the deterioration of the disease and the occurrence of shock, DIC and so on. Therefore, anti-pancreatic enzyme therapy has drawn increasing attention, some people think that is the treatment of acute pancreatitis, the center of medical therapy. First, the anti-pancreatic enzyme therapy principle of action: the destruction of pancreatic activation is mainly through the trypsin and pancreatic lipase digestion. Elastin Activation of Elastin Elastin breaks blood vessels and causes pancreatic bleeding. Phospholipase A activation of phospholipase A lecithin into lysolecithin, lysophospholipid destruction of the cell membrane caused by pancreatic necrosis and necrosis of the fat. Kininogen activation for a variety of kinins, especially bradykinin, can cause visceral vasodilation, increased permeability, hypovolemia