This investigation and others have demonstrated that the development of decidual tissue (DT) in laboratory animal models can be suppressed by the inhibition of prostaglandin (PG) synthesis, and alternatively, DT can be induced by PGs or their precursor, arachidonic acid. The theory that PGs are essential components in the series of events following the induction of the decidual cell response will be examined in this study. This investigator's experience with the technique of uterine vein cannulation, which is essential to this study, will allow us to monitor changes in uterine PGE and PGF production (RIA) prior to dilution in peripheral blood. These studies will be done over a 24 hour period after the induction of DT during the sensitive period. In further studies using the same methods, we will determine if the refractory state is due to an inability of the uterus to respond with an increase in PG production. We have recently shown that DT-bearing pseudopregnant (DT-PSP) rats are resistant to a variety of luteolytic interventions which rapidly terminate PSP in hysterectomized rats. The second half of this study is designed to test the possibility that PGs (particularly of the E series) may be mediators of the luteotrophic action of DT. Small osmotic pumps, only recently available, will be used to produce a tonic release of PGs in H-PSP to determine if they will protect against luteolytic interruption as does DT. Further studies will examine the direct action of PGEs on corpora lutea function in vivo, as well as the possible anti-luteolytic role when administered with PGF2a. The significance of these studies lies in the further definition of causative factors in DT induction, a process similar in both rat and human and essential to reproduction. Information on the luteotrophic action of DT is imperative to full understanding of its role in reproductive physiology.