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作 者:董家鸿[1] 黄志强[2] 王敖川[1] 韩本立[1] 李昆[1] 段恒春[1] 陈莉[1]
机构地区:[1]第三军医大学西南医院肝胆外科中心,重庆400038 [2]解放军总医院普通外科研究所,北京100853
出 处:《中国普外基础与临床杂志》2000年第2期66-68,共3页Chinese Journal of Bases and Clinics In General Surgery
摘 要:目的 探讨胆源性脓毒症时肝脏能量代谢改变的病理特征。方法 借助兔自身对照性动物模型 ,对胆源性脓毒症状态下肝脏线粒体呼吸功能及肝组织ATP含量进行动态检测。结果 自术后 12小时起 ,感染肝叶线粒体Ⅲ态呼吸率 (S3 )、呼吸控制比 (RCR)及磷氧比呈进行性显著降低 ;至术后 48小时氧化与磷酸化脱耦联。非感染肝叶线粒体RCR呈先升后降的双相改变。感染和非感染肝叶组织内ATP含量与其线粒体呼吸活性同步降低。结论 胆源性脓毒症早期即发生肝脏能量代谢障碍 。Objective To investigate the pathological characteristics of hepatic energy metabolism changes due to biliary sepsis. Methods The hepatic mitochondrial respiratory function and content of ATP was dynamically measured in the self controlled rabbit model of biliary sepsis. Results The mitochondrial S 3, respiration control rate (RCR) and phosphorus/oxygen (P/O) were significantly dropping in the infective hepatic lobe 12 hrs after operation with S 4 increasing markedly, and the oxidative phosphorylation was uncoupled from 48 hrs after operation onward. The hepatic mitochondrial RCR showed early ascending and then dropping in the non infective hepatic lobe. The content of ATP and mitochondrial respiratory activity decreased synchronously in both hepatic lobes.Conclusion The hepatic energy metabolic failure was induced in the early stage by biliary sepsis. This is probably the pathological basis of biliary sepsis that is highly critical and always lead to MOF following acute liver function failure.
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