Cunningham C C, Spach P I
Department of Biochemistry, Wake Forest University Medical Center, Winston-Salem, North Carolina 27157-1016.
Alcohol Clin Exp Res. 1994 Feb;18(1):132-7. doi: 10.1111/j.1530-0277.1994.tb00892.x.
A review of the effects of chronic ethanol consumption on myocardial energy metabolism in animal models reveals that alterations in cardiac function are not accompanied by changes in the levels of the high-energy metabolites, ATP, and creatine phosphate. There are minor alterations in mitochondrial ultrastructure and function that appear to be accentuated by lowered nutrient intake. Observations to date indicate that, in animal models, there is an interaction between chronic ethanol consumption and caloric deprivation in eliciting alterations in myocardial energy metabolism. Furthermore, ethanol-related ultrastructural changes and depressed mitochondrial function are much more demonstrable in liver than in heart, suggesting strongly that the myocardium is less susceptible to the deleterious effects of alcohol than is the liver.
对动物模型中慢性乙醇摄入对心肌能量代谢影响的综述表明,心脏功能的改变并未伴随着高能代谢产物、三磷酸腺苷(ATP)和磷酸肌酸水平的变化。线粒体超微结构和功能存在轻微改变,而营养摄入降低似乎会加剧这些改变。迄今为止的观察表明,在动物模型中,慢性乙醇摄入与热量剥夺之间存在相互作用,从而引发心肌能量代谢的改变。此外,与乙醇相关的超微结构变化和线粒体功能抑制在肝脏中比在心脏中更明显,这强烈表明心肌比肝脏对酒精的有害影响更不敏感。