Increased activity of group II phospholipase A2 in plasma in rat sodium deoxycholate induced acute pancreatitis

被引:13
作者
Furue, S
Hori, Y
Kuwabara, K
Ikeuchi, J
Onoyama, H
Yamamoto, M
Tanaka, K
机构
[1] Shionogi & Co Ltd, Discovery Res Labs 2, Toyonaka, Osaka 561, Japan
[2] Shionogi & Co Ltd, Dev Res Labs, Toyonaka, Osaka 561, Japan
[3] Kobe Univ, Fac Med, Dept Surg 1, Kobe, Hyogo, Japan
关键词
acute pancreatitis; phospholipase A(2); sodium deoxycholate pancreatitis; hepatic failure;
D O I
10.1136/gut.41.6.826
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background-Two different types of secretory phospholipase A(2) (PLA(2)), pancreatic group I (PLA(2)-I) and non-pancreatic group II (PLA(2)-II), have been identified and postulated to be associated with the pathogenesis of various diseases, such as acute pancreatitis, septic shock, and multiple organ failure. Aims-To investigate the type of secretory PLA(2) responsible for its catalytic activity found in plasma and ascites of experimental acute pancreatitis. Methods-Acute pancreatitis of differing severity was induced by the injection of different concentrations (1% or 10%) of sodium deoxycholate (DCA) into the common biliopancreatic duct in rats, and catalytic PLA(2) activity in plasma and ascites were differentiated by anti-PLA(2)-I antibody and specific inhibitor of PLA(2)-II. Survival rate and plasma amylase, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were also measured. Results-In 1% and 10% DCA induced acute pancreatitis, plasma amylase values as well as PLA(2) activity in ascites were greatly increased. PLA(2) activity in plasma was also notably increased in 10% DCA induced acute pancreatitis, but not in 1% DCA induced acute pancreatitis. PLA(2)-I specific polyclonal antibody significantly inhibited PLA(2) activity in ascites but not that in plasma. In contrast, plasma PLA(2) activity was completely suppressed by PLA(2)-II specific inhibitor. In addition, a high mortality (93% at five hours) and a significant increase in plasma AST and ALT were noted in 10% DCA induced pancreatitis. Conclusion-Ascites PLA(2) activity is mainly derived from PLA(2)-I, whereas plasma PLA(2) activity is mostly derived from PLA(2)-II in severe acute pancreatitis, suggesting that increased plasma PLA(2)-II activity might be implicated in hepatic failure arising after severe acute pancreatitis.
引用
收藏
页码:826 / 831
页数:6
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