Poor Spontaneous and Oxytocin-Stimulated Contractility in Human Myometrium from Postdates Pregnancies
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Prolongation of pregnancy i.e. going more than 10 days over the estimated due date, complicates up to 10% of all pregnancies and is associated with increased risk to both mother and fetus. Despite the obvious need for contractions of the uterus to end pregnancy, there have been no studies directly examining the role of uterine smooth muscle, myometrium, in the aetiology of prolonged pregnancy. This study tested the hypothesis that the intrinsic contractile characteristics of myometrium taken from women with prolonged pregnancy (>41 weeks and 3 days) was reduced compared to those delivering at term (39–41 weeks). We recruited women undergoing Caesarean Section (CS) delivery either pre-labour (n = 27) or in labour (n = 66) at term or postdates. The contractile ability of the postdates myometrium, whether spontaneous or elicited by oxytocin or high-K solution, was significantly reduced compared to term myometrium. These differences remained when adjusted for parity and other maternal characteristics. The findings remained significant when expressed per cross sectional area. Histological examination revealed no differences between the two groups. The contractile differences were however related to intracellular Ca transients suggesting an effect of [Ca] on reduced force production in the postdates group. In summary, myometrium from prolonged pregnancies contracts poorly in vitro even when stimulated with oxytocin and in active labour. Responses to high K+ and measurements of Ca suggest that alterations in excitation contraction coupling, rather than any histological changes of the myometrium, may underlie the differences between term and postdates myometrium. We show that postdates pregnancy is associated with poor myometrial activity and suggest that this may contribute to increased myometrial quiescence and hence, prolonged gestation.Keywords:
Myometrium
Contractility
Uterine contraction
Uterine contraction pressures were quantified (in Montetevideo units) in 109 women at term gestation who received oxytocin for induction or augmentation of labor and whose labor resulted in a spontaneous vaginal delivery. Newborn five-minute Apgar scores were greater than or equal to 8 in 108 of the 109 neonates, and no immediate neonatal morbidity was attributable to the oxytocin stimulation of labor. Women undergoing oxytocin induction had significantly greater uterine contraction pressures than those with oxytocin augmentation. During oxytocin induction 91% of women achieved at least 200 to 224 Montevideo Units and 40% at least 300 Montevideo units versus 77 and 7.7%, respectively, during augmentation of labor. With concurrent fetal monitoring these levels of uterine activity should be sought before consideration of a cesarean delivery because of presumed cephalopelvic disproportion or failure to progress.
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Abstracts The bioactivity of an oxytocin‐like substance in human term placental tissue was examined using rat uterine muscle obtained during diestrus. The human term placental tissue extract contracted the rat uterine muscle on a Magnus apparatus. Placental tissue extract incubated with oxytocin antiserum did not induce significant contraction of the muscle, whereas placental tissue extract incubated with normal rabbit serum induced a significant effect on the rat uterine muscle. Synthetic oxytocin caused contraction similar to that caused by placental tissue extract in rat uterine muscle. This contraction was also inhibited when synthetic oxytocin was incubated with anti‐oxytocin serum for 24 hr at 4°. Normal rabbit serum and anti‐oxytocin serum alone did not cause contraction. These results suggest that the oxytocin‐like substance in the human placenta may possess uterine contractile activity.
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In this paper, we applied a new theoretical model of uterine contraction to a large panel of human pregnant and nonpregnant myometrial strips, treated or not by corticotrophin-releasing hormone (CRH). This model is based on a fine analysis of the contraction curves. This analysis yielded four mathematical parameters (beta, theta, tau 1, and tau 2) related to excitability, duration of plateau phase, and time constants for relaxation describing, respectively, the different portions of the contraction cycle. This leads to specific differences in spontaneous contractile activity between pregnant and nonpregnant states. The relaxing effect of CRH in the pregnant state is presumably correlated with the origin of the strips (the lower uterine segment). Besides our observation of a specific receptor-dependent relaxing effect of CRH in both pregnant and nonpregnant myometrium, we could identify highly significant effects at given CRH concentration for beta in nonpregnant myometrium and for theta, tau 1, and tau 2 in pregnant myometrium. In addition, highly significant differences were found between pregnant and nonpregnant myometrium. Also, we discovered a strong correlation between theta and tau 1, specifically in the pregnant state. Although the biochemical signification of these results remains to be elucidated, they contribute to emphasize the complex network of CRH action at the myometrial level. Furthermore, our approach could pave the way toward a better analysis of the efficacy of the uterine contractile behavior.
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The effect of instenon upon the uterine contractile activity was studied in pregnant rats. The drug administration at a dose resulted in significant suppression of the myometrium contractility. The effect was not decreased when instenon was injected against the background of oxytocin. On the other hand, the concurrent injection of oxytocin upon a single or long-term administration of instenon produced a pronounced stimulating action on the myometrium contractility.
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Aim To establish and optimize the dysmenorrhea model of oxytocin induced in vitro uterine contraction in mice. Methods Several kinds of estrogen used to enhance the sensibility of mouse uterus were compared, the uterus was separated from the body, 0.5~10 U·L-1 oxytocin was used to induce uterine contraction, the variations after changing treatment were observed, and four parameters used to described the uterine contraction were compared. Results Oxytocin in the concentration of 5 U·L-1 was the suitable dose; the contractions were constant 5~30 min after oxytocin was given; the sensibility of uterus showed a little decrease but was not significant when body weight increased; the contractions were stable 5~30 min after oxytocin was given; the activity of uterus was completely suppressed by 1 mg·L-1 verapamil, 100 μg·L-1 nifedipine and 250 μg·L-1 chloropromazine. Conclusion Oxytocin induced in vitromouse uterine contraction model was a convenient, quick and stable in vitro dysmenorrhea model, suitable for screening dysmenorrhea therapy drugs.
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In brief Various etiologies can cause uterine myometrium contraction, which leads to preterm birth. This study demonstrates a new functional relationship between the Ras-related C3 botulinum toxin substrate 1 (RAC1) and uterine myometrium contraction in preterm birth. Abstract Preterm birth (PTB) is a public health issue. The World Health Organization has recommended the use of tocolytic treatment to inhibit preterm labour and improve pregnancy outcomes. Intrauterine inflammation is associated with preterm birth. RAC1 can modulate inflammation in different experimental settings. In the current study, we explored whether RAC1 can modulate spontaneous uterine myometrium contraction in a mouse model of lipopolysaccharide (LPS)-induced intrauterine inflammation. Subsequently, we recorded uterine myometrium contraction and examined uterine Rac1 expression in a mouse model of preterm birth and a case in pregnant women by Western blotting analysis. We also measured progesterone levels in the blood serum of mice. Murine myometrium was obtained 12 h post LPS treatment. Human myometrium was obtained at the time of caesarean section. We found that in the LPS-treated group of mice, uterine myometrium contraction was enhanced, protein levels and activation of RAC1 were increased and serum progesterone levels were decreased. The protein levels of RAC1 were also increased in preterm birth and in pregnant women. NSC23766, a RAC1 inhibitor, attenuated uterine myometrium contraction and diminished RAC1 activation and COX-2 expression. Furthermore, silencing of RAC1 suppressed cell contraction and COX-2 expression in vitro . In conclusion, our results suggested that RAC1 may play an important role in modulating uterine myometrium contraction. Consequently, intervening with RAC1 represents a novel strategy for the treatment of preterm birth.
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