Abstract
We hypothesized that modest maternal ethanol intake would deleteriously affect developing fetal myocardium. Pregnant guinea pigs were given either water (C), n=13, or 2½% ethanol (EtOH), n=11, for the last 1/2 of pregnancy (12% of calories). At birth, progeny body and heart weights were measured, and cardiac sarcoplasmic reticulum (SR) was isolated for determination of Ca++ uptake, Ca++ binding, and Ca++ stimulated ATPase.
Maternal mortality was not significantly different between groups: 0% in C, 18.2% in EtOH (p>0.10). Litter sizes, proportion of progeny born alive, and progeny body weights in C and EtOH were similar (p>0.10). Despite similar body weights, heart weight/body weight ratios of EtOH's were less than C's: 4.16 ±0.65 (n=38) vs 4.61 ±0.66 (n=29) gm/kg (p<0.005). Ca++ flux was also less in EtOH's than C's: Ca++ uptake 132 ±23 (4) vs 209± 4 (5) nM/mg Pr/min (p 0.001); Ca binding 26 ± 8 (5) vs 53 ± 2 (5) nM/mg Pr/4 min (p<0.001); Ca++ stimulated ATPase 0.7 ± 0.3 (5) vs 1.2 ±.01 (5) μM/mg Pr/10 min (p<0.01).
Modest consumption of ethanol during pregnancy significantly alters Ca++ flux in isolated cardiac SR of the newborn guinea pig. These findings are similar to those observed in adults with alcoholic cardiomyopathy. These data suggest that altered cardiac excitation-contraction may contribute to the production of certain features of the fetal alcohol syndrome.
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Tobin, J., Noren, G., Surdy, J. et al. BIOCHEMICAL EVIDENCE OF CARDIOMYOPATHY IN GUINEA PIGS EXPOSED IN UTERO TO ALCOHOL. Pediatr Res 18 (Suppl 4), 146 (1984). https://doi.org/10.1203/00006450-198404001-00319
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DOI: https://doi.org/10.1203/00006450-198404001-00319