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作 者:蒲青凡[1] 孙碎康[1] 严律南[2] 金凯[1] 蔡宇[1] 余瑞立[1] 戴华卫[1]
机构地区:[1]浙江省瑞安市人民医院外二科,325200 [2]华西医科大学附属第一医院普外科
出 处:《上海医学》2002年第2期80-82,共3页Shanghai Medical Journal
摘 要:目的 探讨钙稳态与前列腺素类异常在急性水肿性胰腺炎 (AEP)向坏死性胰腺炎 (ANP)发展过程中的作用。方法 采用胰管结扎、外分泌刺激诱发大鼠AEP ,在AEP模型基础上静脉注射大剂量高分子右旋糖酐Dextran 110 (5 0 0mg/kg)诱发ANP ,应用荧光探针Fura2 /AM直接测定胰腺泡细胞胞质游离钙离子浓度([Ca2 + ]i) ,并观察血浆前列腺素类 :血栓素A2 (TXA2 )、前列环素 (PGI2 )的变化。结果 ANP模型后腺泡细胞胞质游离钙离子浓度呈持续增高 (P <0 .0 5 ) ,同时血浆TXA2 水平也明显增高 (P <0 .0 5 ) ,而血浆 6 keto PGF1α无明显变化 (P >0 .0 5 )。Objective The aim of this work was to establish a relationship between calcium homeostasis and prostanoids in the conversion of acute edematous pancreatitis(AEP) to necrotizing pancreatitis(ANP) in rats. Methods Cytosolic free Ca 2+ concentration([Ca 2+ ] i) in isolated pancreatic acinar cells,and plasma prostanoid production (thromboxane B 2,6 keto prostaglandin F 1α) were studied in two models of pancreatitis in rats.AEP was induced by pancreatic duct ligation and exocrine stimulation. ANP was induced same as AEP but with a larger dose of Dextran 110(500mg/kg) intravenously. Results The results showed that pancreatic acinar cell [Ca 2+ ] i increased consistently after induction of ANP,and plasma TXB 2 increased significantly with respect to AEP.Conclusion The present results indicate that calcium homeostsis may play an important role and may be responsible,in part,for prostanoid enhanced biosynthesis in the conversion of AEP to ANP in rats.
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