Alcohol (eth) consumption during pregnancy may result in fetal alcohol syndrome (FAS) which includes cardiac defects and myocardial contractile dysfunction. To understand mechanism of FAS associated cardiac defects, we analyzed the effects of maternal chronic alcohol consumption on the expression of fetal myosin heavy chain (MHC) gene that encodes one of the major cardiac contractile protein and exists in α and β isoforms, encoded by separate genes. Timed pregnant Sprague-Dawley rats were randomly assigned to 4 groups on day 1 gestation. Three groups received 10%, 20% and 30% eth (v/v) respectively ad libitum for drinking for 20 days. Control group had regular drinking water. Eth consumption was recorded daily. Mean eth consumption(absolute) during 20 day treatment was 71 ± 5, 110 ± 6 and 126± 5 ml in 10%, 20% and 30% groups respectively. On day 20 gestation, blood alcohol levels were measured, body weights recorded and rats were sacrificed. A total of 21 pregnant rats and 170 fetuses were studied. Blood eth levels ranged 150-250 mg/100 ml in treated groups. Body weight gain in control group was 158 ± 6 gm, in eth groups it was 141 ± 19, 93± 15 and 30 ± 12 gm with 10%, 20% and 30% groups respectively. Effect of eth on steady state levels of α- and β-MHC mRNA was tested in fetal hearts by Northern blot analysis using 32P labeled oligonucleotide probes synthesized from 3′ untranslated regions of respective genes. Steady-state level of α-MHC mRNA showed dose related decline in eth groups compared to controls. β-MHC mRNA remained unchanged in 10% group but decreased in 20% and 30% eth groups. Our data suggest that decreased expression of MHC may partly be responsible for the cardiac defects and contractile dysfunction in FAS.