Home About us Contact | |||
Uterine Contractility (uterine + contractility)
Selected AbstractsThe Physiological Basis of Uterine Contractility: A Short ReviewEXPERIMENTAL PHYSIOLOGY, Issue 2 2001S. Wray In this review we discuss our current understanding of the cellular basis of uterine contractility, highlighting those areas requiring further study. It is clear that the basic processes of excitation-contraction coupling lie within the myometrial cell, and that these may be modified by agonists. Pacemaker acitivity, however, remains a mystery. The contribution of extracellular calcium entry to contraction is shown to be vital, whilst the role of the sarcoplasmic reticulum remains controversial. Much current experimental focus is on pathways controlling and regulating contraction, and we discuss sensitisation mechanisms and question their role in intact uterine preparations. [source] Functional MR imaging of the female pelvisJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 6 2007Takashi Koyama MD Abstract Recent developments in MR techniques have magnified the roles and potential of MRI in the female pelvis. This article reviews the techniques and clinical applications of functional MRI (fMRI) of the female pelvis, including cine MRI, diffusion-weighted MRI (DWI), and dynamic contrast-enhanced (DCE)-MRI. Cine MRI is a useful tool for evaluating uterine contractility, including sustained contraction and peristalsis, in a variety of conditions and gynecologic disorders, and for evaluating pelvic-floor weakness. DWI can demonstrate abnormal signals in pathologic foci based on differences in molecular diffusion. It also enables the quantitative evaluation of the apparent diffusion coefficient (ADC), which may be useful for distinguishing malignant from benign tissues and monitoring therapeutic outcome. DCE-MRI has the potential to improve tumor detection and local staging, and can also provide quantitative information about perfusion of the tumor, which may be useful for both monitoring therapeutic effects and predicting therapeutic outcome. Understanding the roles played by functional MR techniques in the female pelvic region is beneficial not only for determining clinical applications, but also for developing further investigations with MRI. J. Magn. Reson. Imaging 2007;25:1101,1112. © 2007 Wiley-Liss, Inc. [source] Psychological and Physiological Stress: Impact on Preterm BirthJOURNAL OF OBSTETRIC, GYNECOLOGIC & NEONATAL NURSING, Issue 5 2003FAAN professor, Susan Gennaro DSN Stress increases corticotropin-releasing hormone and may ultimately result in increased uterine contractility. Stress also increases cytokine production, which independently may lead to preterm birth or increase susceptibility to infection, thereby increasing the risk of preterm birth. Finally, stress may change health behaviors that lead to preterm birth. Research findings on the relationship between stress and preterm birth have been contradictory. In this article, the authors propose a model of the relationship between stress and preterm birth, evaluate the research on stress and pregnancy outcomes, and discuss the implications for nursing practice and research. [source] Depletion of membrane cholesterol eliminates the Ca2+ -activated component of outward potassium current and decreases membrane capacitance in rat uterine myocytesTHE JOURNAL OF PHYSIOLOGY, Issue 2 2007A. Shmygol Changes in membrane cholesterol content have potent effects on cell signalling and contractility in rat myometrium and other smooth muscles. We have previously shown that depletion of cholesterol with methyl-,-cyclodextrin (MCD) disrupts caveolar microdomains. The aim of this work was to determine the mechanism underlying the increase in Ca2+ signalling and contractility occurring in the myometrium with MCD. Patch clamp data obtained on freshly isolated myocytes from the uterus of day 19,21 rats showed that outward K+ current was significantly reduced by MCD. Membrane capacitance was also reduced. Cholesterol-saturated MCD had no effect on the amplitude of outward current suggesting that the reduction in the outward current was due to cholesterol depletion induced by MCD rather than a direct inhibitory action of MCD on the K+ channels. Confocal visualization of the membrane bound indicator Calcium Green C18, revealed internalization of the surface membrane with MCD treatment. Large conductance, Ca2+ -sensitive K+ channel proteins have been shown to localize to caveolae. When these channels were blocked by iberiotoxin outward current was significantly reduced in the uterine myocytes; MCD treatment reduced the density of outward current. Following reduction of outward current by MCD pretreatment, iberiotoxin was unable to produce any additional decrease in the current, suggesting a common target. MCD treatment also increased the amplitude and frequency of spontaneous rises in cytosolic Ca2+ level ([Ca2+]i transients) in isolated myocytes. In intact rat myometrium, MCD treatment increased Ca2+ signalling and contractility, consistent with previous findings, and this effect was also found to be reduced by BK channel inhibition. These data suggest that (1) disruption of cholesterol-rich microdomains and caveolae by MCD leads to a decrease in the BK channel current thus increasing cell excitability, and (2) the changes in membrane excitability produced by MCD underlie the changes found in Ca2+ signalling and uterine contractility. [source] Effects of LPS and IL-6 on Oxytocin Receptor in Non-Pregnant and Pregnant Rat UterusAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2000XIN FANG PROBLEM: Little is known regarding the regulation of the timing of parturition. Recent evidence suggests an interaction between the immune system and uterine contractility in late gestation. METHOD: Pregnant rats were treated with LPS in vivo in attempts to establish a model of premature parturition induced by the pro-inflammatory response. Uterine explants were incubated in vitro to determine the effects of IL-6 on uterine synthesis of oxytocin (OT) and its receptor (OTR). RESULTS: LPS injection was quite toxic to pregnant rats and gave extremely variable results. In animals that delivered, there was a marked increase in the uterine concentrations of OTR and OTR mRNA. There was no consistent effect regarding the timing of parturition. IL-6 caused a significant increase in the concentration of OTR mRNA in uterine explants from pregnant rats but not in tissues from non-pregnant animals. CONCLUSION: Rat uterine concentrations of OTR are regulated by IL-6. Pro-inflammatory cytokines may stimulate uterine contractility in late gestation rat uterine tissues through a mechanism involving stimulation of OTR. [source] Poor uterine contractility in obese womenBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 10 2007U Kiran No abstract is available for this article. [source] Poor uterine contractility in obese womenBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 3 2007J Zhang Objective, The aim of the study was to elucidate the reason for the high rate of caesarean section in obese women. We examined the following hypotheses: (1) obese women have a high incidence of complications related to poor uterine contractility,caesarean section for dysfunctional labour and postpartum haemorrhage. 2) The myometrium from obese women has less ability to contract in vitro. Design, First, a clinical retrospective analysis of data from 3913 completed singleton pregnancies was performed. Secondly, in a prospective study the force, frequency and intracellular [Ca2+] flux of spontaneously contracting myometrium were related to the maternal body mass index. Setting, Liverpool Women's Hospital and University of Liverpool. Population, The clinical study involved all women who delivered in one hospital in 2002. The in vitro study myometrial biopsies were obtained from 73 women who had elective caesarean section at term. Results, Maternal obesity carried significant risk of caesarean section in labour that was highest for delay in the first stage of labour (OR 3.54). The increased risk of caesarean section in obese women largely occurred in women with normal- and not with high-birthweight infants. Obese women delivering vaginally had increased risk of prolonged first stage of labour and excessive blood loss. Myometrium from obese women contracted with less force and frequency and had less [Ca2+] flux than that from normal-weight women. Conclusions, We suggest that these findings indicate that obesity may impair the ability of the uterus to contract in labour. [source] The history of tocolysisBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 2003Marc J.N.C. Keirse In 1950, the World Health Organisation (WHO) defined prematurity as a birthweight of 2500 g or less and in 1961 as a gestational age of less than 37 weeks. The time in between marks an era in which there was growing recognition of the importance of gestational age at birth and how to influence it. The latter was facilitated too by the development of tocography, which permitted some semi-objective measurement of uterine contractility. Along with it, came a growing interest in agents that could control uterine contractility beyond the earlier classical approaches of hormones and gastrointestinal spasmolytics. Hence, the early 1960s saw much research interest in agents, such as nylidrine, isoxsuprine, and orciprenaline that could suppress uterine contractility as one of their many beta-agonist properties. Subsequently, two approaches would be used to shift the balance towards uterine function over and above the influence on other bodily functions. One consisted of supplementing these drugs with agents, such as calcium antagonists and beta-receptor blockers that were hoped to suppress non-uterine actions. The other was a search for drugs in the same class with greater uterospecificity and more selective binding to uterine as opposed to other receptors. Neither of these approaches has ever fully fulfilled the hopes that were pinned on them, but they resulted in the availability of a large number of agents to suppress uterine contractility. The advent of prostaglandins as regulators of uterine contractility and the ability to suppress their biosynthesis saw another range of attempts to suppress uterine activity. They included aspirin, sodium salicylate, flufenamic acid, sulindac and indomethacin, but some were clearly based on a defective understanding of how uterine prostaglandin synthesis can be influenced. In the meantime, a flurry of other agents came and went, often more than once, testifying to the ingenuity of clinicians in trying to solve a problem that is poorly understood. Some, such as relaxin and ethanol, came and disappeared. Others, such as calcium antagonists, entered the scene as protectors against the non-uterine effects of other agents, went, and re-entered the scene in their own right. Still others, such as magnesium sulphate, came, lingered around, and became credited with effects in preterm labour that do not depend on affecting uterine contractility. Amidst this all arose the term tocolysis, coined in 1964 by Mosler from the Greek stems ,,,,' and ,,,,,,', to epitomise all of this ingenuity. [source] Postpartum intrauterine pressure studies of the uterotonic effect of oral misoprostol and intramuscular syntometrineBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2001Y.S. Chong Objectives To investigate the effect of oral misoprostol in dosages varying from 200 ,g to 800 ,g on postpartum uterine contractility and to establish their side effects. Design A prospective descriptive study. Participants Fifty-seven women who delivered vaginally after spontaneous labours not requiring augmentation. Methods Within 5 minutes of delivery of the placenta, a calibrated Gaeltec catheter with an intrauterine pressure transducer at its tip was inserted transcervically into the uterine cavity. Cumulative uterine activity was recorded for 30 minutes in each woman before administering the oral misoprostol tablets and continued for a further 90 minutes after its administration. Thus each woman acted as her own control regarding changes in uterine contractility. Uterine activity was recorded on a Sonicaid Meridian fetal monitor, which measures active contraction area automatically. The incidence of side effects was also recorded. Results There was no statistical difference (P=0.887) in the adjusted mean difference in cumulative uterine activity following all the doses of oral misoprostol, compared with intramuscular syntometrine, the largest difference being seen in oral misoprostol 200 ,g (adjusted mean difference ,2282 kPas s, 95% CI ,7954 to 3390 kPas s). The mean onset of action of oral misoprostol (6.1, SD 2.1 min) was significantly slower than that of intramuscular syntometrine (3.2, SD 1.5 min; P=0.002), but their durations of action were similar (P=0.637). In the misoprostol group the commonest side effects were shivering (36%) and a rise in body temperature above 38°C (40%). In the syntometrine group, the most commonly observed side effect was moderate uterine pain (nine out of ten women) and a rise in diastolic blood pressure of 20 mmHg (two out of ten women). Conclusion The results of this study show that oral misoprostol has a definite uterotonic effect on the postpartum uterus. At doses of 200 ,g to 400 ,g, oral misoprostol has a similar uterotonic effect to intramuscular syntometrine. Higher doses of oral misoprostol are associated with significantly more side effects. [source] |