Disease relevance of Uterine Contraction

• Cervical laceration, laceration or rupture of the lower uterine segment, retention of the placenta, and hemorrhage in part reflect the intensity of uterine contraction induced by dinoprost [1].
• Bacterial infection induces an inflammatory response characterized by elevated production of proinflammatory cytokines; the latter activate the production of both PGs that stimulate uterine contractions, and matrix metalloproteinases (MMPs) that degrade the extracellular matrix of the chorioamniotic membranes [2].
• Two women treated with sulpiride reported mild uterine contractions, but no spontaneous abortion occurred in either group [3].
• We conclude that DES acts in the rat to depress the preterm levels of steroid hormones, which leads to a failure of uterine contraction accompanied by placental detachment and fetal death [4].
• Although the mechanisms responsible for the onset of preterm labor in human pregnancy are unclear, animal studies have demonstrated that decreased nutrient intake is associated with increased uterine prostaglandin F metabolite production and spontaneous uterine contractions [5].

High impact information on Uterine Contraction

• BACKGROUND: Patients with upper gastrointestinal ulceration may be treated with misoprostol, but it is not recommended for pregnant women because it may stimulate uterine contractions and cause vaginal bleeding and miscarriage [6].
• Initiation of uterine contractions by disopyramide during pregnancy [7].
• Oxytocin may therefore stimulate uterine contractions by acting both directly on the myometrium and indirectly on decidual prostaglandin production [8].
• In this coordinated manner, the uterine contractions that culminate in delivery of the fetus may proceed uninterrupted in the face of increased cortisol production [9].
• At term under the influence of oxytocin there is a modification in the coupling mechanisms that leads to a decrease in the biological activity of the CRH receptor and in the generation of cyclic adenosine monophosphate which favours myometrial contractions [10].

Chemical compound and disease context of Uterine Contraction

• Progesterone (n = 72) and placebo (n = 70) groups were compared for epidemiologic characteristics, uterine contraction frequency, and incidence of preterm birth [11].
• The fetal responses to the PGE2-induced uterine contraction were a bradycardia which was apparent within 10 seconds (P less than 0.05), and a hypertension which was also apparent within 10 seconds (P less than 0.03) [12].
• These results suggest that 1-deamino-[D-Tyr(Oethyl)2,Thr4,Orn8] vasotocin, unlike ritodrine, is a potent and specific antagonist of oxytocin-induced uterine contractions and thus may have potential clinical utility in the treatment of preterm labor [13].
• OBJECTIVES: Our purpose was to determine the effect of magnesium sulfate infusion on nonlabor uterine contractures and corticotropin-induced preterm uterine contractions in pregnant sheep [14].
• CONCLUSIONS: Magnesium sulfate infusion in pregnant sheep has no effect on either nonlabor uterine contractures or on corticotropin-induced preterm uterine contractions [14].

Biological context of Uterine Contraction

• 106 women between 24 and 33 weeks' gestation and in preterm labour, rigidly defined to include cervical dilatation plus regular uterine contractions, were randomly allocated to receive either intravenous ritodrine hydrochloride or no tocolytic treatment [15].
• Androstenedione treatment of pregnant baboons at 0.7-0.8 of gestation promotes a premature forward shift in the nocturnal maternal plasma estradiol surge relative to progesterone and increases myometrial contraction activity [16].
• The increased production of bradykinin in the uterus on the day of parturition could play a significant role in the mechanism responsible for activation of uterine contractions during this event [17].
• Significant increases of PGF2 alpha and PGFM in the peripheral plasma were observed when the frequency of uterine contraction reached a maximum, about 1 h before ovulation [18].
• Although neurohypophyseal OT release has long been associated with uterine contraction and milk ejection, the function of intracerebral OT remains unclear [19].

Anatomical context of Uterine Contraction

• In addition, stimulated amnion membrane produces both PAF and prostaglandin E2, each of which is capable of inducing myometrial contraction [20].
• Parathyroid hormone-related protein (PTHrP) is a smooth muscle relaxant that inhibits myometrial contractions and therefore may act in synergy with progesterone to maintain myometrial quiescence during late pregnancy [21].
• Kallikrein-induced rat uterine contractions as well as bradykinin-induced contractions were enhanced by rat submandibular gland bradykinin potentiating factor [22].
• The findings suggest that cervical softening by fluprostenol does not result from a simple direct action on the cervix or by increasing uterine contractions, but rather by an indirect hormonal action mediated by the ovaries [23].
• Arachidonic acid is mobilized from fetal membrane phospholipids at parturition leading to increased production of oxytocic prostaglandins which may initiate or maintain myometrial contractions [24].

Associations of Uterine Contraction with chemical compounds

• The data suggest that uterine contraction produced by a homologous kallikrein does not involve kinin formation but results from an action of this serine proteinase upon other accessible systems coupled to the contractile response [25].
• All the patients were treated with beta-sympathomimetic infusion, either salbutamol (0.4-1.6 mg/h) or ritodrine hydrochloride (2-6 mg/h), to stop uterine contractions, and with intramuscular dexamethasone 4 mg eight hourly to accelerate foetal lung maturity [26].
• PTHrP-(1-34) reduced the magnitude of acetylcholine-stimulated uterine contraction [27].
• Whether uterine contractility is increased or decreased by adrenergic stimulation is determined by the gonadal steroids estrogen and progesterone: uterine contraction prevails in the estrogen-dominant or the ovariectomized animal, but in the progesterone-dominant rabbit, uterine relaxation is observed [28].
• PGE2 is known to induce uterine contraction by increasing intracellular Ca2+ [29].

Gene context of Uterine Contraction

• 4. BQ-3020 (10(-11)-3 x 10(-7) M) did not cause uterine contraction; neither did it affect the dose-response curve of ET-1 for either the contractile effect or the increase in oscillation frequency [30].
• In media conditioned by chorion, the initiation of uterine contractions did not change MMP activity or TIMP-1 levels [31].
• The abundance of DSCR1 and TCTE1L mRNA was attenuated when myometrial contraction was inhibited by Nimesulide (n=6), a specific prostaglandin H synthase 2 inhibitor [32].
• The abundance of ECE-1 in the basal plate is consistent with a second possible function of this enzyme in affecting uterine contractions [33].
• Effect of interleukin 2 on the production of progesterone and prostaglandin E2 in human fetal membranes and its consequences for preterm uterine contractions [34].

Analytical, diagnostic and therapeutic context of Uterine Contraction

• A significant correlation between the density of OT receptors and the frequency of uterine contractions (external tocography) was found in pregnant women before surgery [35].
• CONCLUSIONS: Bolus administration of intravenous ephedrine reversed the dramatic decrease in diastolic uteroplacental blood flow velocity and the increase in resistance index during uterine contraction, without altering fetal hemodynamic parameters [36].
• BACKGROUND: Ambulatory epidural analgesia (AEA) is a popular choice for labor analgesia because ambulation reportedly increases maternal comfort, increases the intensity of uterine contractions, avoids inferior vena cava compression, facilitates fetal head descent, and relaxes the pelvic musculature, all of which can shorten labor [37].
• The effect of four semi-purified compounds obtained from Mandevilla velutina crude extract by silica gel chromatography fractionization were analysed for their inhibitory effects on uterine contractions induced by bradykinin (BK), lysylbradykinin (L-BK), acetylcholine (ACh) and oxytocin, in vitro [38].
• One hundred twenty women from 20 to 36 weeks' gestation with a complaint of labor who had more than four uterine contractions per hour after intravenous hydration but no evidence of cervical changes were randomized to receive a 2-hour intravenous infusion of atosiban at a rate of 300 micrograms/min or placebo [39].

References