Jaatinen P I, Saukko P, Sarviharju M, Kiianmaa K, Hervonen A
Department of Public Health, University of Tampere, Finland.
Alcohol Alcohol. 1994 May;29(3):269-82.
The myocardial interactions of ageing and lifelong ethanol ingestion were studied in the ethanol-preferring AA (Alko Alcohol) line of rats. Samples of the left ventricle from young control rats (3-month), old control rats (30-month) and rats exposed to ethanol from 3 to 30 months of age, were studied in terms of myocardial ultrastructure and lipopigmentation. Electron microscopic morphometry showed an age-related increase in the volumetric densities of lipofuscin and unspecified sarcoplasm, while the proportions of mitochondria, myofibrils and tubular structures remained unaltered in the left ventricular myocardium. Lifelong ethanol exposure increased the proportion of sarcoplasmic reticulum and transverse tubules, apparently due to dilation of the tubular structures. Mitochondria were significantly larger in the ethanol-exposed rats compared to the control rats of the same age, while the volumetric proportion of mitochondria tended to decrease in the ethanol-exposed group. Fluorescence microscopic image analysis showed that myocardial lipopigmentation (proportion of myocardial area covered by autofluorescent lipopigments) was about two-fold in the old ethanol-exposed rats compared to the old control rats, and 13-fold compared to the young controls. It is concluded that ageing and chronic ethanol ingestion produce rather different patterns of alteration in myocardial ultrastructure, which does not support the concept of ethanol-induced accelerated ageing. The enhancement of myocardial lipofuscin accumulation is thought to reflect chronic oxidative stress in the hearts exposed to ethanol.
在嗜酒的AA（阿尔科酒精）品系大鼠中研究了衰老与终生摄入乙醇对心肌的相互作用。对年轻对照大鼠（3个月）、老年对照大鼠（30个月）以及3至30个月龄接触乙醇的大鼠的左心室样本进行了心肌超微结构和脂褐素沉着方面的研究。电子显微镜形态计量学显示，左心室心肌中脂褐素和未明确的肌浆的体积密度随年龄增长而增加，而线粒体、肌原纤维和管状结构的比例保持不变。终生接触乙醇会增加肌浆网和横小管的比例，这显然是由于管状结构的扩张。与同龄对照大鼠相比，接触乙醇的大鼠线粒体明显更大，而接触乙醇组中线粒体的体积比例有下降趋势。荧光显微镜图像分析显示，与老年对照大鼠相比，老年接触乙醇的大鼠心肌脂褐素沉着（自发荧光脂褐素覆盖的心肌面积比例）约为两倍，与年轻对照大鼠相比则为13倍。结论是，衰老和慢性乙醇摄入在心肌超微结构中产生的改变模式差异较大，这并不支持乙醇诱导加速衰老的概念。心肌脂褐素积累的增强被认为反映了接触乙醇的心脏中的慢性氧化应激。
