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|本期目录/Table of Contents|

螺内酯对截肢创伤致大鼠心肌线粒体损伤的拮抗

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第3期
页码:
296-299
栏目:
基础研究
出版日期:
2009-05-15

文章信息/Info

Title:
Mechanism of myocardial mitochondria injury and protection of spironolactone after traumatic amputation
作者:
陈亚巍; 谢晓华; 任青爱; 张海峰; 张颖
解放军总医院综合外一科，北京 100853
Author(s):
CHEN Ya-wei;  XIE Xiao-hua;  REN Qing-ai;  ZHANG Hai-feng;  ZHANG Ying
First Department of Comprehensive Surgery, PLA General Hospital, Beijing 100853, China
关键词:
心肌; 线粒体; 截肢; 创伤性; 醛固酮; 螺内酯
Keywords:
myocardium;  mitochondria;  amputation; traumatic;  aldosterone;  spironolactone
分类号:
Q577
DOI:
-
文献标识码:
A
摘要:
目的 研究创伤后大鼠心肌线粒体呼吸功能的改变及螺内酯干预的效果。方法 采用手术的方法建立大鼠左后肢截肢创伤模型，雄性SD大鼠24只，随机分为正常对照组（仅麻醉）、创伤对照组（麻醉后截肢）和螺内酯组（20mg/Kg的螺内酯连续灌胃6 d，麻醉后截肢），每组8只,观察各组大鼠心肌线粒体呼吸控制率(respiratory control ratio,RCR)、磷氧比值(oxidative phosphorylation ratio、P/O)、总ATP酶、膜电位(mitochondrial transmembrane potential,ΔΨm)的变化。结果 创伤对照组RCR、P/O、总ATP酶和ΔΨm， 均较正常对照组显著降低(P<0.01)，与创伤对照组比较，螺内酯干预后，RCR、总ATP酶和ΔΨm均得到改善(P<0.05)， P/O变化不显著。结论 截肢创伤可导致心肌线粒体功能下降，螺内酯干预可减轻线粒体损伤，提示醛固酮可能参与了创伤后心肌线粒体的损伤。
Abstract:
AIM To investigate the effects of aldosterone on the respiration of myocardial mitochondria and of spironolactone on the protection after traumatic amputation. METHODS The model of traumatic amputation was established by surgery. Twenty-four male SD rats were randomly divided into 3 groups (n=8): control group (only anesthesia), trauma group (anesthesia and amputation) and spironolactone group (6-day 20 mg/kg spironolactone intragastric administration and then amputation). The respiratory control ratio (RCR), oxidative phosphorylation ratio (P/O), total ATP enzyme and mitochondrial transmembrane potential（ΔΨm） in myocardial mitochondria were determined 6 hours after amputation. RESULTS The RCR, P/O, total ATP enzyme and ΔΨm in the trauma group were significantly lower than those in the control group (P<0.01). Compared with those in trauma group, the RCR, total ATP enzyme and ΔΨm in the spironolactone group were higher (P<0.05) and no significant changes were found in P/O. CONCLUSION The function of myocardial mitochondria is impaired after trauma and spironolactone can attenuate the impairment. Adlosterone may participate in the myocardial mitochondria aggravation after trauma.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2008-10-20.基金项目：军队“十一五”科技攻关课题基金资助（06G117） 通讯作者：谢晓华，主任医师，主要从事心血管系统的围手术期治疗研究Email: n4xxh@126.com 作者简介：陈亚巍，医师，硕士生Email: tjcywei1981@yahoo.cn
更新日期/Last Update: 2009-05-18