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作 者:蒋建新[1] 汪江淮[1] 陈惠孙[1] 胡德耀[1] 刁有芳[1] 田昆仑[1]
机构地区:[1]第三军医大学野战外科研究所,重庆630042
出 处:《中国药理学与毒理学杂志》1992年第1期64-66,共3页Chinese Journal of Pharmacology and Toxicology
摘 要:采用大鼠单侧股骨粉碎性骨折伴15%体重失血的模型,观察动物存活率,肝脏线粒体呼吸控制率(RCR),ADP/O值的变化以及ia TRH 5 mg·kg^(-1)对肝线枉体呼吸功能的保护作用,创伤休克时,肝脏线粒体RCR,ADP/O值显著降低,24 h大鼠存活率明显减少,TRH能明显提高肝线粒体RCR,ADP/O值以及休克动物存活率,提示TRH有明显改善休克大鼠肝线粒体氧化磷酸化功能的作用。This experiment studied the protective effects of thyrotropin releasing hormone (TRH) on rat hepatic mitochondria following traumatic shock induced by the right femural comminute fracture with the blood loss of 15% the body weight by examining the survival rate and RCR and ADP / O values of the liver mitochondria. The results showed that a significant fall in RCR and ADP / O values occurred after traumatic shock, the administration of TRH 5 mg·kg-1 could obviously increase RCR and ADP/ O values and the survival time of the shock animal, andTRH could improve the mitochondrial respiratory function for a long time. Therefore, it is suggested that TRH could significantly improve oxidative phosphorylation of the hepatic mitochondria in shock animals and increase the synthesis and supply of intracellular energy. So TRH may protect cellular damage during shock.
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