The influence of the fetal genome on trypan blue‐induced cardiovascular defects

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Abstract
The mean litter incidence of genetically determined, congenital patencies of the interventricular cardiac septum was found to differ significantly and consistently in control neonates produced by matings within and between two Long‐Evans lines of rats (O/O>C/O>O/C>C/C). When dams carrying siblings of control neonates were injected with a standardized dose of trypan blue on day 8 of pregnancy, there occurred significant increases in the incidence of cardiovascular malformations in litters of all genotypes. Although neither the magnitude of the increases nor the severity of the induced malformations was directly correlated with line or sibship differentials with respect to the incidence of spontaneous septal, patencies some unidentified aspect of the fetal genome significantly influenced the nature of the induced defects. Both O/O and hybrid litters were characterized by a high incidence of severe transposition syndromes, consistently associated with highly specific, unilateral cephalic malformations or extensive spina bifida. The incidence of comparable associated head and heart malformations was significantly lower in C/C litters, in many of which the dye exposure merely increased the incidence of isolated interventricular septal patencies over that found in control siblings or induced noncardiovascular malformations at the caudal end of the body axis. In general, the collective data afford little support for the concept that a familial or subline predisposition towards spontaneously occurring cardiac malformation renders the fetal cardiovascular system particularly susceptible to the teratogenic activity of trypan blue.