胰腺缺血在胰腺炎由水肿向坏死转变中的研究  

Acting mechanism of pancreatic ischemia in the conversion of acute edematous pancreatitis to necrotizing pancreatitis in rats

作　　者：蒲青凡 严律南[1,2,3,4] 刘占培[1,2,3,4] 谭建三 左凤琼[1,2,3,4] 吴兆锋 

机构地区：[1]攀枝花市攀钢密地医院外科 [2]华西医科大学附属第一医院普外科 [3]华西医科大学公共卫生学院 [4]华西医科大学基础医学院

出　　处：《中国冶金工业医学杂志》1999年第2期67-70,共4页Chinese Medical Journal of Metallurgical industry

摘　　要：目的：本实验旨在研究急性水肿性胰腺炎（ＡＥＰ）向坏死性胰腺炎（ＡＮＰ）转变中胰微循环障碍的作用机理。方法：将９６只大鼠随机分三组：Ⅰ组，假手术组；Ⅱ组，采用胰管结扎及静脉推注蛙皮素（１００μｇ／ｋｇ）、促胰液素（１０μｇ／ｋｇ）诱发ＡＥＰ；Ⅲ组，在ＡＥＰ模型同时静注１０％高分子右旋糖酐（分子量１１００００）５００ｍｇ／ｋｇ诱发ＡＮＰ。应用荧光探针Ｆｕｒａ２研究钙超负荷情况。结果：发现ＡＮＰ模型后１、３、６、９小时腺泡细胞胞浆游离钙离子浓度持续增高（Ｐ＜００５），而胰腺细胞质膜Ｃａ２＋－ＡＴＰａｓｅ活性持续降低（Ｐ＜００５）。结论：细胞钙超负荷可能介导胰腺缺血性损害促使ＡＥＰ向ＡＮＰ转变。Objective:The acting mechanism of pancreatic ischemia in the conversion of acute edematous pancreatitis(AEP) to necrotizing pancreatitis(ANP) was studied.Methods:Ninety six Sprague Dawley rats were randomized in three experimental groups as follows:(GroupⅠ)Shamoperated control.(Group Ⅱ)AEP was induced by pancreatic duct ligation and intravenous injection of bombesin(100 μg/kg)and secretin(10 μg/kg).(Group Ⅲ)ANP was induced same as group Ⅱ but with a large dose of dextran 110000(500 mg/kg)intravenously.Pancreatic acinar cell Ca 2+ overload was studied using fluorescent probe fura 2.Cytoslolc free Ca 2+ concentration([Ca 2+ ] i) in isolated pancreatic acinar cells and Ca 2+ -ATPase activity in pancreatic cell plasma membranes were determined 1h,3h,6h,9h after treatment.Results:The results showed that pancreatic acinar cell [Ca 2+ ] i was elevated at 1h(212 93±19 27 nM,P<0 05) and increased to 463 76±29 10 nM at 6h(P<0 05) in rats with ANP,pancreatic cell plasma membrane Ca 2+ -ATPase activity decreased significantly from 29 81±0 43(Pinmol/mg.prot/min) at 1h to 18 61±0 46(Pi nmol/mg.prot/min) at 9h in rats with ANP(P<0 05).Conclusions:The Ca 2+ overload mediated pancreatic ischemic injury may induce the conversion of AEP to ANP.

关 键 词：胰腺炎 局部缺血 钙超负荷 机理 病理 

分 类 号：R657.510.2[医药卫生—外科学]