ABSTRACT
The mechanism for parturition in women remains a mystery, but in most cases delivery occurs following the spontaneous onset of labor at around 39-41 weeks of gestation. It is not known whether women who go into labor and deliver preterm do so as a consequence of a different physiopathological mechanism, or as a result of the mis-timing or acceleration of the same process that operates at term. From a practical point of view, it is useful to subdivide preterm deliveries (deliveries at 37 weeks of gestation) into very early preterm birth (32 weeks of gestation) and extremely preterm birth (28 weeks of gestation) because the rates of perinatal mortality or disability in the newborns are considerably different in each subgroup.1,2 The prevention of all preterm births is an unattainable goal because this would mean resolving every medical and obstetric complication of pregnancy (e.g. pregnancy-induced hypertension; pre-eclampsia, antepartum hemorrhage, premature rupture of the membranes). These complications contribute to iatrogenic preterm deliveries. However, by focusing our efforts on spontaneous preterm labor we have the potential to improve neo - natal mortality and morbidity rates quite substantially. Our ignorance of the mechanism of parturition at term, let alone preterm labor, has made this very difficult; and the prevention of preterm labor remains the most important challenge in obstetrics in the 21st century. In this chapter the role of prostaglandins (PG) and oxytocin (OT) in human labor, and the rationale behind the use of PG and OT antagonists in an attempt to stop preterm labor, are reviewed.
