Uphoff C, Nyquist-Battie C, Toth R
Teratology. 1984 Aug;30(1):119-29. doi: 10.1002/tera.1420300116.
The purpose of the present research was to determine the effect of in utero ethanol exposure on cardiac muscle development. Pregnant albino mice (Swiss strain) at 8 days of gestation were divided into three groups: a normal group fed Purina lab chow for rodents and water ad libitum; an ethanol group fed the liquid diet ENSURE with 20% of the calories derived from ethanol (12.6 +/- 1.2 gm/kg body weight per day); and an isocaloric group pairfed ENSURE with 20% of the calories derived from sucrose. These diets were continued until birth, at which time the litter size, crown to rump length, and weight were recorded. Randomly selected neonatal pups from each litter were decapitated and their hearts immediately processed for transmission electron microscopy. Litter size, crown to rump length, and body weight of the ethanol-treated mice at birth were significantly less than normal but not less than pairfed controls. Ultrastructural evaluation of cardiac muscle from mice treated in utero with ethanol in comparison to that from both normal and pair-fed control animals revealed various degrees of morphological alterations. The most pronounced alterations were in mitochondrial structure and included an increase in mitochondrial volume per cytoplasmic volume and a marked decrease in the amount of inner mitochondrial membrane. Myofibrillar abnormalities were also evident in the ethanol group but not in either control group. These abnormalities included a decrease in the myofibril volume per cytoplasmic volume and a disruption in myofibril organization particularly the Z-bands. The ultrastructural alterations in the cardiac muscle from the ethanol treated group were not a result of malnutrition or dehydration as the pairfed group did not exhibit these changes. It is apparent from this study that exposure of mice in utero to ethanol can cause ultrastructural abnormalities in cardiac muscle cells. Whether these changes result in heart pathophysiology and persist to adulthood are not known.
本研究的目的是确定子宫内乙醇暴露对心肌发育的影响。妊娠8天的怀孕白化小鼠（瑞士品系）被分为三组：正常组，自由采食普瑞纳啮齿动物实验室饲料并随意饮水；乙醇组，喂食含20%热量来自乙醇的液体饮食安素（每天12.6±1.2克/千克体重）；等热量组，配对喂食含20%热量来自蔗糖的安素。这些饮食持续到出生，此时记录产仔数、顶臀长度和体重。从每窝中随机选择新生幼崽断头，其心脏立即用于透射电子显微镜检查。乙醇处理组小鼠出生时的产仔数、顶臀长度和体重显著低于正常组，但不低于配对喂食对照组。与正常和配对喂食对照动物相比，子宫内用乙醇处理的小鼠心肌的超微结构评估显示出不同程度的形态学改变。最明显的改变是线粒体结构，包括每细胞质体积中线粒体体积增加以及线粒体内膜数量显著减少。乙醇组中肌原纤维异常也很明显，但对照组均未出现。这些异常包括每细胞质体积中肌原纤维体积减少以及肌原纤维组织紊乱，尤其是Z带。乙醇处理组心肌的超微结构改变不是营养不良或脱水的结果，因为配对喂食组没有出现这些变化。从这项研究可以明显看出，子宫内乙醇暴露可导致小鼠心肌细胞超微结构异常。这些变化是否会导致心脏病理生理学改变并持续到成年尚不清楚。
