Transient cranial hemorrhage does not cause depressed contractility in cardiac neural crest-ablated chick embryos.

Ablation of cardiac neural crest results in cardiovascular malformations. Depressed ventricular contractility has been noted in cardiac neural crest-ablated embryos several hours before the time when neural crest cells would have arrived in the cardiac outflow tract and several days before the appearance of any malformations. The reason for this depressed heart function is not known. Recently, transient cranial hemorrhages were found in chick embryos during the third day of incubation, several hours before depressed ventricular contractility can be measured. We sought to determine whether depressed ventricular contractility could be associated with these transient hemorrhages. We were also interested in defining some of the factors that influence the incidence and severity of hemorrhaging. Three groups of embryos were used: cardiac neural crest-ablated, sham-operated, and unopened controls. All groups were found to experience transient hemorrhage from a common origin in the forebrain. However, the incidence and degree of hemorrhage were higher and more severe in embryos with cardiac neural crest ablation than in the other two groups. The cardiac ejection and shortening fractions were measured at stage 18 in embryos with and without hemorrhaging, and it was found that a decrease in these parameters was associated solely with ablation of cardiac neural crest and not with hemorrhage. By altering the incubation conditions, we determined that conditions that increase the oxygen in the air space are associated with increased severity and occurrence of hemorrhage and decreased viability in the first 3 days of incubation. Our results indicate that transient cranial hemorrhages does not cause depressed contractility in cardiac neural crest-ablated embryos, and increased severity of hemorrhaging is most likely due to an increase in oxygen availability.