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作 者:董家鸿[1] 黄志强[1] 王敖川[1] 程绍钧[1] 付国金[1] 尹国清 段恒春[1] 李昆[1] 陈莉[1]
机构地区:[1]重庆第三军医大学西南医院肝胆外科
出 处:《中华实验外科杂志》1995年第4期199-200,共2页Chinese Journal of Experimental Surgery
基 金:全军青年科学基金
摘 要:于兔右侧叶肝管开口近端结扎肝总管,并向其近端肝管内注入2×10 ̄8E·coli/0.2ml大肠杆菌菌液,从而诱发脓毒症。在伤后12、24和48h采取动脉血用糖氧化酶法测定血糖含量;用放免法测定血浆胰高糖素、皮质醇和胰岛素的浓度。伤后12h动物血糖显著升高,至伤后24h血糖转而持续降低。血乳酸水平进行性升高。血胰高糖素水平持续显著升高;血皮质醇水平在伤后12~24h显著升高,至48h降至正常;而血胰岛素水平变化不显著。上述结果表明,兔胆源性脓毒症时血糖水平呈早期高血糖继以持续低血糖的双相反应;低血糖相不依赖于促进糖异生的激素环境和底物水平,可能是肝细胞水平上糖异生途径抑制的结果。This study charaterized the matabolic, glucoregulatory,hormonal responses to biliarysepsis in fasted rabbits,Biliary sepsis in rab-bits was induced by ligation of the bile duct ata point just above the junction of the right lat-eral hepatic duct with the common bile ductand injection of live E. coli suspansion contain-ing 2×10  ̄6 organisms into the proximal bileduct.Plasma levels of glucose,lactate,glucagon,insulin,and cortisol were measuredat 12,24 and 48 hour following septic chal-lenge. Rabbits with biliary sepsis displayed anearly mild hyperglycemia,but rapidly pro-gressed to profound hypoglycemia within 24hours post septic challenge. Persistant hyper-lactacidemia was observed since 12 hours.In-sulin levels were stable,whereas,glucagonlevels were progressively elevated over the 48hrs period.Cortisol levels increased duringfirst 24 hr post sepsis,then decreased towardcoatrol levels late into the septic course,Thesedata indicate that hypoglycemia develop inspite of the substrate and hormonal profilesprevailing in the cells’s envioronment thatgreatly favored accelerated gluconeogenesiswhich may result from the depression of hep-atic gluconeogenesis.
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