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Fetal alcohol effects on the postnatal development of the rat myocardium: an ultrastructural and morphometric
P H Syslak1, E J Nathaniel, C Novak
1Department of Anatomy, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Insights
Prenatal ethanol exposure in rats causes significant heart muscle damage in offspring, affecting myofibril development. These cardiac ultrastructural changes in fetal alcohol syndrome are most severe early postnatally but show some recovery by 21 days.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Toxicology
Background:
- Heart disease is a common complication of fetal alcohol syndrome.
- Understanding the impact of prenatal ethanol exposure on cardiac development is crucial.
Purpose of the Study:
- To investigate the postnatal ultrastructural effects of in utero ethanol exposure on rat cardiac muscle.
- To characterize the temporal changes in myocyte morphology following prenatal alcohol exposure.
Main Methods:
- Time-pregnant Sprague-Dawley rats were fed ethanol or a control diet.
- Offspring were surrogate-fostered by normal dams post-birth.
- Cardiac muscle ultrastructure was analyzed at 7, 14, and 21 days postnatal.
Main Results:
- Ethanol-exposed pups exhibited reduced body weight and crown-rump length.
- Myocyte damage, particularly to myofibrils, was observed, peaking at 7 days postnatal.
- Delayed M-band development and reduced myofibril volume density were noted in ethanol-exposed pups by 21 days.
Conclusions:
- In utero ethanol exposure significantly disrupts postnatal cardiac muscle ultrastructural development in rats.
- Myofibril dysplastic changes and developmental delays are key findings.
- While damage is evident early, some recovery of myocyte structure occurs by 21 days postnatal.
Abstract:
Heart disease is an entity frequently seen in the fetal alcohol syndrome. This paper describes the effect of in utero ethanol exposure on the postnatal ultrastructural development of rat cardiac muscle. To determine this time-pregnant Sprague-Dawley rats were fed either a nutritionally balanced protein- and vitamin-enriched liquid ethanol diet (with 36% of the calories derived from ethanol) or a liquid diet with maltose-dextrins isocalorically substituted for ethanol. The latter group was designated the pairfed control group. At birth, pups of both the groups were surrogate-fostered by normal dams. Body weights and crown-rump lengths were significantly less in the rat pups exposed to ethanol in utero at 21 days postnatal. Ultrastructural analysis of the cardiac muscle was performed at 7, 14, and 21 days postnatal in ethanol and pairfed groups. Several morphological features of myocyte damage were observed in ethanol-exposed pups, predominantly at 7 days postnatal, with nearly total absence of myocyte damage by 21 days postnatal. The most outstanding changes were observed in the myofibrils, which showed dysplastic changes at 7 days postnatal, a delay in M-band structural development at 14 days postnatal, and a significantly smaller myofibril volume density per tissue volume at 21 days postnatal in the ethanol rat pups compared to the pairfed controls.