Diverse observations indicate that decidual prolactin interacts locally with relaxin, cytokines, and PGs and potentially with other decidual peptides such as oxytocin, growth factors, and corticotropin-releasing hormone, all of which are acknowledged mediators of parturition. The addition of prolactin to human fetal membrane preparations significantly blunted PGE2 production but increased plasminogen activator activity.
Taken together, these findings suggest that decidual prolactin alone, or in concert with other peptides and autocoids, functions as a regulatory factor in primate parturition and that changes in amniotic fluid prolactin may reflect decidual activation—i.e., the endogenous release of proinflammatory mediators or a localized withdrawal of progesterone action at the matemo-fetal interface. Alternatively, changes in amniotic fluid prolactin may simply reflect the sequelae of parturition. According to the latter theory, the accumulation of PGs and cytokines in amniotic fluid is an aftereffect of labor and cervical dilatation whereby the fetal membranes and attached decidual fragments are exposed and bathed by microbial products in the vaginal fluid. ventolin inhalers
Careful longitudinal measurements of amniotic fluid prolactin are necessary to answer these questions.