NO对心肌细胞线粒体功能影响的病理生理学意义  

Effects of nitric oxide on mitochondrial function in cardiomyocytes:pathophysiological relevance

作　　者：魏星[1] 康毅[2] 刘欣[1] 

机构地区：[1]天津医科大学病理生理教研室,天津300070 [2]天津医科大学药理学教研室,天津300070

出　　处：《中国病理生理杂志》2009年第8期1656-1659,共4页Chinese Journal of Pathophysiology

摘　　要：It is now clear that both endogenous and exogenous sources of nitric oxide(NO) exert important modulatory effects on cardiac mitochondrial function.There is also growing evidence that NO can be produced within the mitochondria themselves.NO can influence respiratory activity,both through direct effects on the respiratory chain or indirectly via modulation of mitochondrial calcium accumulation.At pathological concentrations,NO causes irreversible alterations in respiratory function and also interacts with reactive oxygen species(ROS) to form reactive nitrogen species(RNS),which may further impair mitochondrial respiration and even lead to open the mitochondrial permeability transition pore and induce cell death.Diabetes,aging,myocardial ischemia,and heart failure are all associated with altered ROS generation,which can alter the delicate regulatory balance of effects of NO in the mitochondria.It is now clear that both endogenous and exogenous sources of nitric oxide （NO） exert important modulatory effects on cardiac mitochondrial function. There is also growing evidence that NO can be produced within the mitochondria themselves. NO can influence respiratory activity, both through direct effects on the respiratory chain or indirectly via modulation of mitochondrial calcium accumulation. At pathological conceuirations, NO causes irreversible alterations in respiratory function and also interacts with reactive oxygen species （ROS） to form reactive nitrogen species （RNS）, which may further impair mitochondrial respiration and even lead to open the mitochondrial permeability transition pore and induce cell death. Diabetes, aging, myocardial ischemia, and heart failure are all associated with altered ROS generation, which can alter the delicate regulatory balance of effects of NO in the mitochondria.

关 键 词：一氧化氮 线粒体 心肌细胞 

分 类 号：R363.1[医药卫生—病理学]