Abstract
The evidence which suggests a role for prostaglandins in parturition is reviewed, with special reference to experimental observations on the rat. The pregnant uterus can both synthesize and metabolize prostaglandins. The biosynthetic capacity of the rat uterus increases as pregnancy proceeds. This increase, which is especially marked during the last few days of pregnancy, may be oestrogen-controlled. During pregnancy the tissue levels of the major prostaglandin-metabolizing enzyme, 15-hydroxyprostaglandin dehydrogenase (EC 1.1.1.141) is greatly increased. This may prevent aberrant production of prostaglandins from terminating the pregnancy prematurely. The capacity for prostaglandin metabolism begins to fall (perhaps under hormonal control) as the expected day of delivery approaches; this, coupled with an augmented biosynthesis, produces a net increase in uterine prostaglandins which contribute to the process of parturition by causing a decrease in progesterone concentration, increasing the muscular tone of the uterus, and altering uterine haemodynamics. Agents which block either prostaglandin synthesis or metabolism delay or accelerate the parturition process in the rat.
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