Ethyl alcohol‐induced cardiovascular malformations in the chick embryo

Abstract

Chick embryos incubated for 72-80 hours were exposed to various volumes (0.20-0.40 m1/egg) of 50% ethyl alcohol. Examination of embryos at day 14 of incubation showed that higher doses of ethanol decreased the survival rate of embryos compared with control embryos. Three major categories of cardiovascular malformations were observed in this study: intracardiac anomalies characterized primarily by isolated ventricular septal defect, ventricular septal defect with overriding aorta, double outlet right ventricle or common aorticopulmonary trunk; aortic arch anomalies; and subclavian artery anomalies. Frequencies of embryos with intracardiac anomalies were equal to or greater than 64.8% in the six groups exposed to ethanol. Administration of ethanol also induced high frequencies of embryos with subclavian artery anomalies (11.2-89.1%). Absence or hypoplasia of the right and/or left secondary subclavian artery was commonly associated with persistence of the corresponding primary subclavian artery. Bilateral absence and/or hypoplasia of the secondary subclavian arteries was more common than unilateral anomalies, whereas absence of the left secondary subclavian artery was more commonly observed than an absent right secondary subclavian artery. No embryos in the two control groups combined (n = 94) demonstrated aortic arch or subclavian artery anomalies.

Effects of Light Ethanol Consumption During Pregnancy: Increased Frequency of Minor Anomalies in the Newborn and Altered Contractility of Umbilical Cord Artery

“…It has been shown that in utero ethanol exposure can damage the cardiovascular system (23,24). Hence, we examined its effects on umbilical arteries because these were the only readily available vessels of fetal origin and also because these arteries are fundamental in regulating fetoplacental blood flow.…”

“…In particular, ethanol exposure during embryogenesis can lead to vascular and cardiac abnormalities (23,24). Hence, a second purpose of our investigation was to assess the possible effects of maternal ethanol consumption on the UCAs of the newborns, taking this vessel as a readily available sample of fetal vasculature and inferring that alterations of it may parallel those in other vessels.…”

Fetal Origins of Cardiovascular Disease

“…Myocardial contractility of the fetus decreases quickly after a maternal episode of high alcohol ingestion, an effect that persists for hours [159]. Studies in chick embryos demonstrated a dose dependent effect of ethanol administrated into the yolk sac, since the incidence of ventricular septal defects increased from 43% to 74% when the concentration was raised from 0.2 mL 50% ethanol per egg to 0.4 mL 50% ethanol per egg [160]. In a rat model, oral administration of ethanol to pregnant rats resulted in a decrease in offspring body weight at 21 days old, as well as the heart weight in relation to the respective weights of the body, kidney, and liver [155,161].…”

A tissue culture model for studying ethanol toxicity on embryonic heart cells

“…The interatrial defect occurred in 41% of the offspring of ethanoltreated mothers. Similarly, acute exposure to ethanol early in development produced high incidence of septal defects in both mice and chick embryos (Webster et al, 1984;Daft et al, 1986;Fang et al, 1987). Although these in vivo studies provide evidence that episodic rather than chronic exposure to ethanol may be the underlying cause for cardiovascular defects associated with FAS, the cellular mechanisms involved in the teratogenic process were not determined.…”