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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＜００５），而胰腺细胞质膜Ｃａ２＋－ＡＴＰａｓｅ活性持续降低（Ｐ＜００５）。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: This study was designed to investigate the mechanism of pancreas microcirculation transition in patients with acute edematous pancreatitis (AEP) to necrotizing pancreatitis (ANP). Methods: Ninety - six rats were randomly divided into three groups: group Ⅰ, sham operation group and group Ⅱ. Anesthesia induced by bombardment and intravenous injection of bombesin (100 μg / kg) and secretin (10 μg / kg) In group Ⅲ, ANP was induced by intravenous infusion of 10% macromolecule dextran (molecular weight 110000) 500mg / kg at the same time in AEP model. Fura2 was used to study calcium overload. Results: After 1, 3, 6 and 9 hours of ANP model, the concentration of cytoplasmic free calcium in the acinar cells continued to increase (P <005), while the activity of Ca2 + -ATPase in the plasma membrane continued to decrease (P <005) . Conclusion: Calcium overload may mediate the ischemic injury of the pancreas to promote the transformation of AEP to ANP.