Uterine contraction

About: Uterine contraction is a research topic. Over the lifetime, 1549 publications have been published within this topic receiving 31630 citations. The topic is also known as: contraction.

Uterine contractions at the time of embryo transfer alter pregnancy rates after in-vitro fertilization.

Abstract: To investigate the possible consequences of uterine contractions (UC) as visualized by ultrasound (US) on in-vitro fertilization (IVF)-embryo transfer outcome, we studied prospectively 209 infertile women undergoing 220 cycles of controlled ovarian stimulation. Inclusion criteria were age 5.0 (n = 74) UC/min respectively. Patients, controlled ovarian hyperstimulation and embryology characteristics were comparable in all groups. A stepwise decrease in clinical and ongoing pregnancy rates as well as in implantation rates occurred from the lowest to the highest UC frequency groups (53, 36, 21; 46, 32, 20; 23, 19, 10; and 14, 11, 4%; P < 0.001). Plasma progesterone and UC frequency were negatively correlated (r = -0.34, P < 0.001). Direction of UC did not affect embryo transfer outcome. As this study was controlled strictly for confounding variables and UC were assessed objectively by a computerized system, its results indicate that high frequency UC on the day of embryo transfer hinder IVF-embryo transfer outcome, possibly by expelling embryos out of the uterine cavity. The negative correlation between UC frequency and progesterone concentrations supports the uterine relaxing properties of progesterone.

The dynamics of rapid sperm transport through the female genital tract: evidence from vaginal sonography of uterine peristalsis and hysterosalpingoscintigraphy

Abstract: Vaginal ultrasonography of uterine peristalsis during the follicular phase of the menstrual cycle demonstrates an increasing frequency and intensity of subendometrial and myometrial peristaltic waves as the follicular phase progresses. During this time the numbers of contraction waves with a fundo-cervical direction decrease considerably in favour of waves of contraction with a cervico-fundal direction. There is evidence that rapid sperm transport through the female genital tract is passive and is provided by these uterine contractions. Using hysterosalpingoscintigraphy, rapid sperm transport was studied by placing technetium-labelled albumin macrospheres of sperm size at the external os of the uterine cervix and following their path through the female genital tract. Ascension of the macrospheres occurred immediately following deposition at the external os of the cervix. As early as 1 min thereafter, the macrospheres had reached the intramural and isthmical part of the tube. Quantitatively, the extent of ascension increased with progression of the follicular phase. While only a few macrospheres entered the uterine cavity and even fewer the tubes during the early follicular phase, the proportion of macrospheres that entered the uterine cavity increased dramatically during the mid-follicular phase despite continuing limited entry into the tube. During the late follicular phase there was considerable ascension of the macrospheres which was directed preferentially into the tube ipsilateral to the dominant follicle. These data indicate that rapid transport of the spermatozoa through the female genital tract is under the endocrine control of the dominant follicle, ensuring the preferential accumulation of spermatozoa at the site of fertilization.

Prostaglandins and mechanisms of preterm birth

Abstract: Increased uterine contractility at term and preterm results first from activation and then stimulation of the myometrium. Activation can be provoked by mechanical stretch of the uterus, and by an endocrine pathway resulting from increased activity of the fetal hypothalamic-pituitary-adrenal axis. In sheep fetuses, increased cortisol output during pregnancy regulates expression of prostaglandin synthase type 2 (PGHS-2) in the placenta in an oestrogen-independent manner, resulting in increased concentrations of prostaglandin E2 (PGE2) in the fetal circulation. Later increases in maternal uterine expression of PGHS-2 require increases in oestrogen and lead to increased concentrations of PGF(2alpha) in the maternal circulation. Thus, regulation of PGHS-2 at term is differentially controlled in fetal (trophoblast) and maternal (uterine epithelium) tissue. This difference may reflect expression of glucocorticoid receptor but not oestrogen receptor (ER) in placental trophoblast cells. In women, cortisol also contributes to increased prostaglandin production in fetal tissues through upregulation of PGHS-2 (amnion and chorion) and downregulation of 15-OH prostaglandin dehydrogenase (PGDH; chorion trophoblasts). The effect of cortisol on expression of PGDH in the chorion reverses a tonic stimulatory effect of progesterone, potentially through a paracrine or autocrine action. In membranes, cortisol may be derived from cortisone through activity of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1, in addition to secretion from the maternal or fetal adrenal glands. In placenta, 11beta-HSD-2 oxidase activity predominates and expression of this enzyme is reduced with hypoxaemia and in placentae from pre-eclamptic pregnancies. In these circumstances, increased concentrations of maternal cortisol may cross into the fetal compartment, contributing to growth restriction and programming later life disease.