Strain‐dependent effect of ethanol on ventricular septal defect frequency in white leghorn chick embryos

Abstract

We have tested the potential of a single dose of ethanol (0.20 ml 50% ethanol in chick Ringer's saline (CRS) administered into the air sac) to produce ventricular septal defect (VSD) in three distinct commercially available strains of White Leghorn chick embryo: stress-resistant Dekalb Delta strain, Hy-Vac SPF type V, and Hy-Vac SPF type L. Eggs were controlled for both size and developmental stage (Hamburger-Hamilton stage 18-19) at time of injection. The frequency of VSD in Dekalb Delta embryos was 4.0% (1/25), in Hy-Vac SPF type L embryos 9.1% (3/33), and in Hy-Vac SPF type V embryos 38.9% (14/36). Statistical analysis with the two-tailed Fisher Exact Test indicated that frequencies were not significantly different (P = 0.3215) when Dekalb Delta and Hy-Vac type L embryos were compared. However, the frequency of VSD for Hy-Vac type V embryos was significantly greater than that for either the Dekalb Delta or the Hy-Vac type L embryos (P < 0.005). All VSDs observed were located within the crista supraventricularis. When Hy-Vac SPF type V embryos were exposed to either 0.20 ml 50% ethanol in CRS or to 0.20 ml CRS (controls), ethanol-treated embryos showed a VSD incidence of 34.1% compared with a 3.6% incidence in the controls (P = 0.0017). These data suggest that ethanol is the cause of VSD in this strain. From the results of this study, we are led to conclude that different commercial strains of White Leghorn chick embryo show different susceptibilities to the induction of VSD by ethanol.

Embryonic Ethanol Exposure Dysregulates BMP and Notch Signaling, Leading to Persistent Atrio-Ventricular Valve Defects in Zebrafish

“…In the past three decades, various animal model studies demonstrated that ethanol exposure during development produces heart defects similar to those seen in human [27–31]. Our work illustrated the utility of the zebrafish for studying heart development mechanisms disrupted by ethanol, showing that ethanol exposure during embryogenesis perturbs multiple steps of cardiogenesis, which led to chamber and valve morphogenesis defects [32].…”

Alcohol exposure leads to unrecoverable cardiovascular defects along with edema and motor function changes in developing zebrafish larvae

“…In chick, ventricular septal defect (VSD), double outlet right ventricle and defects in aortic arch and subclavian artery were caused in chick embryos by acute alcohol exposure for 72-80 h (Fang et al, 1987). Bruyere and Stith (1993) studied the effect of alcohol on the hearts of three district commercial strains of White Leghorn chick embryos, and found that the different strains showed different susceptibilities to the induction of VSD by ethanol (Bruyere and Stith, 1993). The defects in embryonic cardiac blood flow during cardiogenesis was associated with the ethanol-induced intracardiac defects in chick embryos (Bruyere and Stith, 1994).…”

Avian Genetic Background Modulates the Neural Crest Apoptosis Induced by Ethanol Exposure

“…Long-Sleep but not Short-Sleep mice are adversely affected by prenatal ethanol exposure with respect to learning deficits (Gilliam et al, 1987), brain weight (Goodlett et al, 1989), and postnatal growth (Gilliam and Kotch, 1996). Chicken strains also exhibit differential susceptibility to in ovo ethanol exposure with respect to mortality, growth, and dose responses (Becker and Shibley, 1998), as well as their sensitivity to cardiac deficits (Bruyere and Stith, 1993;Cavieres and Smith, 2000). The avian findings have particular import given their lack of maternal metabolism or effectors on a uterine environment.…”