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为了探讨急性胰腺炎的发病机制,我们采用胆汁酸盐—胰蛋白酶混合液向胰导管内注射,复制出大鼠急性出血坏死性胰腺炎动物模型。实验结果:在发病后10h动物血浆脂质过氧化物(LPO)即见升高(从4.67上升到20.5nmol/ml),而同时血浆淀粉酶水平已开始下降(从6577降到2629U);心肝、肾、肺组织LPO在术后10、20h也有不同程度的升高(P<0.05或P<0.01)。作者认为:急性胰腺炎时,动物血浆、组织LPO的升高证实了自由基在此病理过程中起着重要作用;与传统用血清淀粉酶水平判断急性胰腺炎发生、发展方法相比较,血浆LPO更能反映出这一病变的发生、发展和全身器官组织受损的程度。
In order to explore the pathogenesis of acute pancreatitis, we used bile acid salt-trypsin mixture to pancreatic ductal injection, replicating animal model of acute hemorrhagic necrotizing pancreatitis in rats. Results: The plasma lipid peroxides (LPO) tended to increase (from 4.67 to 20.5 nmol / ml) at 10 hours after onset, while plasma amylase levels began to decline (from 6577 to 2629 U); heart and liver The levels of LPO in kidney and lung tissue also increased to some extent at 10 and 20 hours after operation (P <0.05 or P <0.01). The author believes that: acute pancreatitis, animal LPO plasma and tissue elevation confirmed the role of free radicals in this pathological process plays an important role; with the traditional serum amylase level to determine the occurrence and development of acute pancreatitis, plasma LPO More reflect the occurrence of this lesion, the development and extent of damage to body organ tissue.