Mitochondrial metabolism following traumatic brain injury in rats.
Mitochondrial metabolism following traumatic brain injury in rats.
复制标题
大鼠脑外伤后的线粒体代谢。
作者：
R. Vink;V. Head;P. Rogers;T. Mcintosh;A. Faden
Although a number of studies of traumatic brain injury have implicated mitochondrial dysfunction as a cause of altered posttraumatic energy metabolism, no studies to date have isolated mitochondria and measured their respiratory capacity following trauma. The present study sought to determine whether mitochondrial capacity for oxidative phosphorylation is adversely affected by fluid-percussion-induced traumatic brain injury in rats. Prior to brain injury, the mitochondrial respiratory control ratio was 4.3 +/- 0.2 and the ratio of nmoles of ADP phosphorylated per natom oxygen consumed (ADP/O ratio) was 2.66 +/- 0.09. After injury (2.8 atm; t = 4 h), there were slight but not significant alterations in ADP/O ratio (2.41 +/- 0.07) and state 3 respiratory rate (ADP stimulated); however, there were no changes in the respiratory control ratio. These data suggest that traumatic brain injury, unlike ischemia, does not cause uncoupling of ATP synthesis from respiration, and that brain mitochondria are quite resistant to trauma-induced injury.
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影响因子：
4.2
作者：
Xiao-Quan Yuan;D. Prough;Thomas L. Smith;D. Dewitt
通讯作者：
Xiao-Quan Yuan;D. Prough;Thomas L. Smith;D. Dewitt
猫轻度实验性头部损伤后的区域脑代谢水平。
影响因子：
4.1
作者：
Yang,MS;DeWitt,DS;Becker,DP;Hayes,RL
通讯作者：
Hayes,RL
DOI：
10.1089/cns.1986.3.257
发表时间：
1986
期刊：
Central nervous system trauma : journal of the American Paralysis Association
影响因子：
--
作者：
H. Kontos;J. Povlishock
通讯作者：
H. Kontos;J. Povlishock
创伤和缺血的损伤后反应：继发性损伤还是保护机制？
DOI：
10.1089/cns.1987.4.27
发表时间：
1987
期刊：
Central nervous system trauma : journal of the American Paralysis Association
影响因子：
--
作者：
Young,W
通讯作者：
Young,W