Investigating the Effect of Extracellular Calcium on Oxytocin-induced Human Myometrial Contractility In-vitro
Status:
Completed
Trial end date:
2015-03-01
Target enrollment:
Participant gender:
Summary
Postpartum hemorrhage (PPH) is a leading cause of maternal morbidity and mortality worldwide
and is caused most commonly by poor uterine muscle tone after delivery. The first line agent
used in the prevention and treatment of PPH is oxytocin, which acts by binding with the
oxytocin receptor (OTR) found on myometrial cells to cause uterine contraction. It does this
by increasing levels of calcium within the myometrial cell, which promotes contraction. Women
who require augmentation of labor with intravenous oxytocin because of inadequate labor
progression have been shown to be at increased risk of PPH. In-vitro human myometrial models
have shown that following prolonged exposure to oxytocin there is desensitization of the
myometrium resulting in a significant reduction in contractility upon delivery of further
oxytocin.
Optimal levels of calcium are very important for contraction of the uterine muscle. Too
little calcium results in a reduced contraction. Too much calcium may result in either
stronger contractions, or even possibly relaxation of the muscle and therefore a reduced
contraction. The investigators currently do not know the effects of calcium on the
desensitized uterine muscle.
The investigators hypothesize that myometrial contractility following desensitization of the
myometrium would be reduced in myometrial samples exposed to low calcium, when compared to
normal calcium or high calcium exposure. These results will help in establishing whether
myometrial contraction can be augmented by increasing calcium levels within the body, or by
optimizing normal physiological calcium levels, in the setting of a augmented prolonged
labor, which is at higher risk of poor uterine contraction and PPH.
Phase:
N/A
Details
Lead Sponsor:
Samuel Lunenfeld Research Institute, Mount Sinai Hospital