Single Cause for Initiation of Labor and Toxemia: A Hypothesis

ABSTRACT

A hypothesis is presented that states that the decline in oxygen tension (PO₂) in the intervillous space causes both toxemia (preeclampsia-eclampsia) and the initiation of labor. The trophoblast is identified as the monitor of the fetal PO₂ and as the source of substances that are released into the maternal circulation stimulating the myometrium, the heart, the vascular smooth muscle, and, perhaps, the brain. In the presence of normal trophoblast the release takes place only when the PO₂ in the intervillous space decreases to a level at which the fetus should be expelled from the uterus to avoid intrapartum hypoxia. Near term, the myometrium is the most responsive site to the released substances, and stimulation of the heart and systemic vasculature is observed only infrequently. With release of these substances, intrapartum toxemia results. Toxemia before onset of labor is created by hypoxia of the trophoblast in the presence of a nonresponsive myometrium to materials released. A small placenta, compression of the intervillous space by villous edema, and avulsion of spiral arterioles are the main causes of the premature decline of intervillous space PO₂, leading to toxemia. Postpartum toxemia is produced by the retained (extraplacental) trophoblast, perhaps facilitated by the rapid clearance of progesterone.