Ohnishi H, Kosuzume H, Ashida Y, Kato K, Honjo I
Dig Dis Sci. 1984 Jan;29(1):26-32. doi: 10.1007/BF01296858.
Therapeutic effect and the mechanism of the action of human urinary trypsin inhibitor (MTI) on experimental acute pancreatitis were studied. MTI significantly increased survival rate of animals with experimental acute pancreatitis induced by the infusion of trypsin or phospholipase A2 into pancreas or by a closed duodenal loop. The efficacy of MTI on these types of pancreatitis were higher than those of aprotinin. Pancreatic enzymes were released from pancreatic slice by trypsin or phospholipase A2, and this release was inhibited by MTI. Further, these pancreatic enzymes caused a secondary release of enzymes from other pancreatic slice, suggesting that these enzymes injured pancreatic tissue and that a chain reaction of pancreatic enzyme activation may play an important role in the pathogenesis of acute pancreatitis. MTI suppressed the secondary enzyme-induced pancreatic injury more strongly than aprotinin. These results suggest that MTI may suppress pathogenesis and development of pancreatitis by inhibiting the chain reaction of pancreatic enzyme activation.
研究了人尿胰蛋白酶抑制剂(MTI)对实验性急性胰腺炎的治疗作用及其作用机制。MTI显著提高了通过向胰腺内注入胰蛋白酶或磷脂酶A2或通过闭合十二指肠环诱导的实验性急性胰腺炎动物的存活率。MTI对这些类型胰腺炎的疗效高于抑肽酶。胰蛋白酶或磷脂酶A2可使胰腺切片释放胰酶,而MTI可抑制这种释放。此外,这些胰酶可导致其他胰腺切片发生酶的二次释放,提示这些酶损伤了胰腺组织,且胰酶激活的连锁反应可能在急性胰腺炎的发病机制中起重要作用。MTI比抑肽酶更强烈地抑制了继发性酶诱导的胰腺损伤。这些结果表明,MTI可能通过抑制胰酶激活的连锁反应来抑制胰腺炎的发病机制和发展。