Abstract
The effects of acute episodes of maternal uterine ischemia on the cardiovascular system of New Zealand white rabbit embryos were studied by in vivo microscopic methods. On gestational day 12, gravid uteri were surgically externalized, and the walls of the implantation sites were carefully incised and reflected to reveal the embryos. Throughout all procedures, temperature, water, and electrolyte homeostasis were preserved. The embryos within each litter were divided into two groups: 1) two randomly selected embryos whose umbilical cords were clamped, and 2) the remaining embryos of the litter whose umbilical cords were uncompromised. Uterine ischemia was induced by clamping all uterine arterial and venous channels. Occlusion of the maternal uterine vessels produced severe uterine cyanosis within 1–2 min. The embryos whose umbilical cords were not clamped exhibited severe cardiovascular derangements beginning within 3–4 min. In contrast, the embryos whose umbilical cords were clamped (thereby interrupting both umbilical and vitelline circulations) had no observable cardiovascular alterations. The absence of effects in embryos with clamped umbilical cords suggests that acute episodes of hypoxia are well tolerated by young embryos. In contrast, the rapid appearance of cardiovascular derangements after interruption of maternal uterine circulation in embryos with undamped umbilical cords emphasizes the idea that even brief intervals of uterine ischemia are deleterious to the rabbit embryo.