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烫伤后心肌线粒体呼吸链变化对心肌收缩性的影响
http://www.100md.com 《中华整形烧伤外科杂志》 1999年第1期
线粒体|烧伤|呼吸链|心肌收缩,关键词:,.,.
烫伤后心肌线粒体呼吸链变化对心肌收缩性的影响

     王志强 蔡宝仁 周卫东 121001 辽宁锦州,解放军第二五医院烧伤整形科 中华整形烧伤外科杂志 1999 0 15 1


    关键词:线粒体;烧伤;呼吸链;心肌收缩 期刊 zhzxsswkzz 0 论 著 fur -->


    

【摘要】 目的 观察重度烧伤对心肌细胞线粒体呼吸链的影响,探讨烧伤后心肌收缩功能下降及心输出量减少的机理。方法 采用30%Ⅲ度烫伤大鼠模型,用差速离心法分离心肌细胞线粒体,以氧电极技术和差光谱法测定琥珀酸呼吸链和还原型辅酶I(NADH)呼吸链的电子传递活性,同时监测心肌力学的变化。结果 烫伤后2h NADH-细胞色素C还原酶及细胞色素氧化酶即低于对照组,烫伤后4 h琥珀酸-Co.Q还原酶、NADH-Co.Q还原酶、琥珀酸-Cyt.C还原酶也明显低于对照组。同时伴心肌收缩功能的下降。但随烫伤时间的延长(烫伤后6h)呼吸链电子传递活性及心肌力学的变化无继续降低。结论 重度烧伤后心肌细胞线粒体呼吸链电子传递活性受到全面损伤,致使心肌氧利用发生障碍,可能是心肌收缩功能下降、心输出量减少的原因之一。

    Effects of thermalinjuryson electron transport chains of rat myocardial mitochondria

WANG Zhiqiang,CAI Baoren,ZHOUWeidong.

    Department of Burns and Plastic Surgery,205th Hospital of People's Liberation Army,Jinzhou121001

Abstract Objective Theelectron transport chain alterations of myocardial mitochondria and cardiac dysfunctionwere studied after severe burn injury.Methods Contraction properties ofmale Sprague-Dawley rat cardiac muscle were investigated at 2,4,6 hours after 30% TBSAfull-thickness thermal injury.Meanwhile,changes in electron transport chains of myocardialmitochondria were measured.Mitochondria were obtained by differential centrifugation.Succinate-respiratory chains and NADH-respiratory chains were assayedpolarographically and spectrophotometrically in isolated myocardial mitochondriarespectively.Results The results showed that thermal injury led todecrease in the activities of two respiratory chains.At 2h postburn, the activities ofNADH-cytochrome C reductase and cytochrome oxidase declined significantly as compared withthat of the sham-operated group, and at 4h postburn,all activities of succinate-Co.Q reductase, succinate-cytochrome C reductase,NADH-Co.Q reductase were much lower than thoseof the sham-operated group. Along with the electron transport chain alterations ofmyocardial mitochondria,there were decrease in myocardial contractile function in burnedrats.Conclusion These results imply that weakness of myocardialcontractile function resulting in the decrease in cardiac output may be associated withthe impairment of utilization of oxygen in myocardial mitochondria following burn injury.

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