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作 者:周蒙滔[1] 张启瑜[1] 施红旗[1] 陈必成[1] 李日千[1] 彭淑牖[1]
机构地区:[1]浙江温州医学院第一附属医院普外科,浙江温州325000
出 处:《肝胆胰外科杂志》2001年第3期149-151,共3页Journal of Hepatopancreatobiliary Surgery
基 金:浙江省医药卫生科研基金项目
摘 要:目的 :探讨早期区域动脉灌注 5 Fu、奥曲肽对急性出血坏死性胰腺炎的治疗机制。方法 :参照Aho法制备杂种犬AHNP模型 ,随机分成四组 :对照组 (A ,n =4)、5 Fu(B ,n =5 )组、奥曲肽 (C ,n =5 )组、5 Fu +奥曲肽 (D ,n =5 )组。之后经胃十二指肠动脉灌注生理盐水、5 Fu、奥曲肽、5 Fu联合奥曲肽 ,并于剖腹前、建立模型时、后 15分钟、1、3、6、10、2 4小时抽血测定血清淀粉酶、α TNF ,血浆TXB2 、6 k PGF1α。结果 :①四组模型前后血清淀粉酶水平明显上升 ,治疗组可使血清淀粉酶水平明显下降 ,其中以D组下降最明显。②对照组模型后 15分钟、1小时血清α TNF水平明显上升 ,治疗组显著下降 ,与模型前相比无明显差别。③四组模型前后TXB2 水平明显上升 ,对照组模型前后血浆 6 k PGF1α水平无明显变化 ,治疗组均有显著上升 ,其中以 5 Fu +奥曲肽组上升最明显。结论 :作用机制可能是 :通过抑制α TNF的合成与分泌 ,从而使AHNP早期过高的血清α TNF水平下降 ;促进 6 k PGF1α的生成 ,从而维持TXA2 和PGI2 之间的平衡 ;抑制淀粉酶的合成与分泌 。Objective:In order to explain the probable mechanism of the regional intraartery infusion with fluorouracil or octreotide or both in the treatment of acute necrotizing hemorrhagic pancreatitis(ANHP).Methods:Nineteen healthy crossbreed dogs were divided randomly into four groups:control group(A),fluorouracil group(B),octreotide group(C),fluorouracil+octreotide group(D). Referring to Aho method,each group was made into the model of AHNP. Then the regional intraartery infusion began instantly,and the blood sample was taken for the measurement of serum amylase,α TNF,plasma TXB 2 and 6 k PGF 1α just before laparotomy and at 15min,1h,3h,6h,10h and 24h respectively after being modeled.Results:①The serum amylase level of each group after being modeled was much higher than that before. Each kind of treatment decreased the serum amylase level,with the most remarkable effectiveness on group D. ②Each kind of treatment reduced the serum α TNF level which was higher than normal at 15min,1h after being modeled. ③The plasma TXB 2 level of each group after being modeled was much higher than that before. Each kind of treatment raised the plasma 6 k PGF 1α level and reduced the ratio of T/K,with the most remarkable effectiveness on the group D.Conclusion:Its probable mechanisms are as follows:The higher level of serum α TNF is reduced by inhibiting the synthesis and secretion of α TNF in early stage. The balance between TXA 2 and PGI 2 is maintained by regulating the metabolism of arachidonic acid and increasing the production of 6 k PGF 1α . The synthesis and secretion of pancreatic enzyme are inhibited.
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