Maternal ethanol consumption induces transient compensatory hyperplasia of developing cardiac tissue in the neonatal rat.

The effect of continuous exposure to ethanol in utero and postpartum on growth and cell division in developing cardiac tissue was studied in neonatal Fischer rats. Pregnant and lactating females were maintained on three dietary regimens; a control group fed rat chow ad libitum, an experimental group receiving an ethanol-containing (6% by volume) liquid diet, and a pair-fed control group, which received an isocaloric amount of control liquid diet. At days 1, 5, and 10 postpartum, five litters of pups from each control and experimental group were sacrificed and the body weights, heart weights, heart-to-body weight ratios, and mitotic frequency of the ventricular myocardium were measured. When compared to either group of controls, pups continuously exposed to dietary ethanol expressed significantly (P < 0.01) lower body weights. Pups maintained by the pair-fed females had significantly (P < 0.01) lower body weights at days 5 and 10 than pups maintained by the chow-fed females, indicating a pair-fed effect of suboptimal nutrition of the model. As the pups developed, the heart weights of pups maintained by the chow-fed females became progressively greater (P < 0.01) than the heart weights of pups maintained by the pair-fed and ethanol-fed females, which expressed no weight difference. The reduction of heart weight present in the ethanol-fed and pair-fed pups represents a pair-fed effect of suboptimal nutrition and not an obvious effect of exposure to dietary ethanol. The ratio of heart weight to body weight and mitotic frequency were significantly greater (P < 0.01) in 1- to 5-day-old pups exposed to ethanol. Following day 5, these parameters decreased and approached the control values. This indicates that growth of cardiac tissue is not suppressed in the 1- to 5-day-old rat pups exposed continuously to dietary ethanol. These observations further suggest the presence of a mechanism intrinsic to the heart which can provide stage-dependent protection from the adverse effects of ethanol during early development. The decline in heart weight to body weight ratios and mitotic frequency in pups of ethanol-fed females also suggests that ethanol may initiate suppression of the growth of cardiac tissue or may incur stage-dependent injury during the later stages of development. The possible mechanism of this stage-dependent protection during early neonatal development is an increased mitotic activity of the cardiac myocytes.