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 postpartumon growth and cell division in developing cardiac tissue wasstudied in neonatal Fischer rats. Pregnant and lactating femaleswere maintained on three dietary regimens; a control group fedrat chow ad libirum, an experimental group receiving an ethanol-containing(6% by volume) liquid diet, and a pair-fed control group, whichreceived an isocaloric amount of control liquid diet. At days1, 5, and 10 postpartum, five litters of pups from each controland experimental group were sacrificed and the body weights,heart weights, heart-to-body weight ratios, and mitotic frequencyof the ventricular myocardium were measured. When compared toeither group of controls, pups continuously exposed to dietaryethanol 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 maintainedby the chow-fed females, indicating a pair-fed effect of suboptimalnutrition of the model. As the pups developed, the heart weightsof pups maintained by the chow-fed females became progressivelygreater (P < 0.01) than the heart weights of pups maintainedby the pair-fed and ethanol-fed females, which expressed noweight difference. The reduction of heart weight present inthe ethanol-fed and pair-fed pups represents a pair-fed effectof suboptimal nutrition and not an obvious effect of exposureto dietary ethanol. The ratio of heart weight to body weightand 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 suppressedin the 1- to 5-day-old rat pups exposed continuously to dietaryethanol. These observations further suggest the presence ofa mechanism intrinsic to the heart which can provide stage-dependentprotection from the adverse effects of ethanol during earlydevelopment. The decline in heart weight to body weight ratiosand mitotic frequency in pups of ethanol-fed females also suggeststhat ethanol may initiate suppression of the growth of cardiactissue or may incur stage-dependent injury during the laterstages of development. The possible mechanism of this stage-dependentprotection during early neonatal development is an increasedmitotic activity of the cardiac myocytes.