Progesterone exerts rapid inhibition of the amplitude of myometrial contractions in vitro but 17OHPC does not. The action of progesterone does not appear to operate via potassium channels nor does it enhance the activity of certain tocolytic drugs.
Maternal obesity is associated with increased rates of labor induction, dysfunctional labor requiring intrapartum cesarean delivery, and postpartum hemorrhage, implying that maternal obesity has an inhibitory effect on myometrial function and its ability to respond to oxytocin. This study aimed to use an in vitro model to investigate the relationship between maternal body mass index (BMI) and the ability of myometrium to contract spontaneously and in response to oxytocin. Linear mixed effects regression modeling was applied to contractile data from 609 strips from 85 women. No correlation was found between maternal BMI and any indices of spontaneous myometrial activity. A single addition of oxytocin increased contractility, however, this was not related to maternal BMI. Similarly, oxytocin concentration-response curves were unrelated to BMI. Overall, the results from this in vitro study suggest that the observed implications of obesity on parturition in vivo cannot be explained by a direct effect on myometrial contractile mechanisms per se.
The observed effects of prolonged in vivo administration of progesterone will minimize the ability of the uterus to contract as a synctium and the ability of peripheral blood leukocytes to migrate into the myometrium during parturition. We suggest that these are putative mechanisms by which progesterone might prevent preterm birth in women at high risk.
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