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1
Bufalino, L., G. Rizzo, D. Rinaldo, E. Romanini, H. Valensise, D. Arduini, and C. Romanini. "Previsione della Preeclampsia nella Gravidanza Gemellare Mediante Velocimetria Doppler Uterina." Acta geneticae medicae et gemellologiae: twin research 43, no. 1-2 (April 1994): 115. http://dx.doi.org/10.1017/s0001566000003056.
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AbstractL'incidenza di pre-eclampsia nella gravidanza gemellare è aumentata di circa 5 volte rispetto alle gravidanze singole. La velocimetria Doppler a livello uterino si è dimostrato in popolazioni a rischio, un metodo efficace per identificare precocemente le pazienti a rischio di pre-eclampsia. Non sono disponibili dati a questo riguardo nella gravidanza gemellare.Obiettivi: 1) valutare le differenze negli indici di resistenza delle arterie uterine tra gravidanze singole e gemellari, 2) valutare eventuali differenze in gravidanze gemellari complicate da pre-eclampsia, 3) valutare il valore predittivo della velocimetria Doppler uterina sulla pre-eclampsia in gravidanze gemellari esaminate a 20-24 settimane di gestazione e poi seguite prospettivamente.Disegno dello studio: l'indice di resistenza RI a livello di entrambe le arterie uterine è stato calcolato mediante Doppler colore-pulsato (Ansaldo Hitachi AU590A) nelle seguenti popolazioni: a) 315 gravidanze singole non complicate, b) 96 gravidanze gemellari non complicate, c) 53 gravidanze gemellari complicate da pre-eclampsia, d) 63 gravidanze gemellari valutate a 20-24 settimane di gestazione e non complicate al momento della osservazione.Risultati: 1) sia nelle gravidanze singole che in quelle gemellari i valori di RI decrescono nel corso della gravidanza e i valori presenti nelle gravidanze gemellari a decorso normale sono significativamente inferiori (Anova p < 0.001). 2) le gravidanze gemellari complicate da preeclampsia dimostrano valori di RI lievemente superiori alle gravidanze gemellari non complicate (p <0.05). 3) il valore predittivo sulla preeclampsia delle arterie uterine a 20-24 settimane è risultato inadeguato (k = 0.24).Conclusioni: la velocimetria Doppler delle arterie uterine è risultata di scarsa utilità clinica nel prevedere la preeclampsia nelle gravidanze gemellari.
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Winata, I. Gede Sastra, and Nicholas Renata Lazarosony. "Procedures to Reduce Haemorrhage during Myomectomy for Fibroids." Cermin Dunia Kedokteran 49, no. 10 (October 3, 2022): 589. http://dx.doi.org/10.55175/cdk.v49i10.2076.
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<p>Uterine fibroids are the most common solid tumors in the female pelvis. Myomectomy is the first choice of treatment for woman who want to keep their uterus. Haemorrhage, uterine perforation, cervical injury, and metabolic problems from excessive absorption of the distension medium, such as glycine, are risks of hysteroscopic myomectomy. There are several procedures and techniques to reduce haemorrhage during myomectomy for fibroids. Some research demonstrated excellent outcomes with uterine artery ligation.</p><p>Mioma uteri adalah tumor jinak yang paling sering dijumpai pada wanita. Tindakan miomektomi adalah salah satu pilihan terapi pada wanita yang tetap ingin mempertahankan rahim. Perdarahan, perforasi uterus, cedera serviks dan masalah metabolisme akibat penyerapan berlebihan media distensi, seperti glisin, adalah risiko prosedur histeroskopi miomektomi. Beberapa prosedur dan teknik dapat mengurangi perdarahan saat miomektomi pada kasus mioma uteri. Beberapa penelitian menunjukkan hasil yang sangat baik dengan ligasi arteri uterina.</p>
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Intriago Cedeño, Carlos Fabricio, Andrea Monserrate Murillo Mera, and Nelson Efren Campoverde Mejia. "Embarazo ectópico cervical: Reporte de caso clínico." QhaliKay. Revista de Ciencias de la Salud ISSN: 2588-0608 3, no. 1 (January 20, 2019): 1. http://dx.doi.org/10.33936/qkrcs.v3i1.2049.
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Los embarazos ectópicos constituyen la emergencia más peligrosa de la gestación en sus primeras etapas. Las presentaciones cervicales comprenden una subcategoría del embarazo ectópico, de naturaleza sumamente infrecuente, con una incidencia del 0,1% de casos, la implantación ocurre en el cérvix en lugar del útero y al ser un sitio de proximidad con las arterias uterinas, la invasión del trofoblasto al cérvix lo convierte en un embarazo ectópico de alto riesgo de compromiso hemodinámico. Se describe el caso de una paciente de 40 años de edad que debuta con cuadro clínico caracterizado por dolor en hipogastrio y fosas iliacas derecha e izquierda, acompañado por amenorrea y sangrado transvaginal, se realizó ecografía transvaginal que muestra la cavidad uterina vacía y una implantación anómala en el cérvix. Se comprobaron los criterios ecográficos de Ushakov, se ratificó la importancia clínica y diagnóstica urgente en esta patología y se instauró el tratamiento conservador quirúrgico de carácter controversial mediante el legrado uterino.
Palabras clave: cérvix, implantación, extrauterino, hemorragia, Ushakov
Abstract
Ectopic pregnancies constitute the most dangerous gestation emergency in its early stages. The cervical presentations include a subcategory of ectopic pregnancy, of a very rare nature, with an incidence of 0.1% of cases, implantation occurs in the cervix instead of the uterus and being a site of proximity to the uterine arteries, the invasion of the trophoblast to the cervix makes it an ectopic pregnancy with a high risk of hemodynamic compromise. We describe the case of a 40 years old patient who debuts with a clinical characterized by pain in hypogastrium and right and left iliac fossae, accompanied by amenorrhea and transvaginal bleeding, transvaginal ultrasound was performed showing the empty uterine cavity and an abnormal implantation in the cervix. The ultrasound criteria of Ushakov were checked, the clinical importance and urgent diagnosis in this pathology were ratified, and conservative surgical treatment of controversial character was established through uterine curettage.
Keywords: cervix, implantation, extrauterine, hemorrhage, Ushakov
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Kokov, L. S., M. M. Damirov, G. E. Belozerov, and O. N. Oleynikova. "Modern approaches to endovascular treatment of uterine leiomyoma." Gynecology 20, no. 5 (October 15, 2018): 63–67. http://dx.doi.org/10.26442/2079-5696_2018.5.63-67.
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Individual features of the blood supply to the uterus and ovaries in 20-25% of cases cause failures in endovascular treatment of patients with uterine leiomyoma (ULM) and are forced to return to traditional surgical methods. The purpose of the study is to assess the possibilities of preventing iatrogenic complications of endovascular treatment of ULM through the use of separating occlusion of the uterine arteries, taking into account the characteristics of the blood supply to the uterus and ovaries. Materials and methods. The work is based on the analysis of the results. X-ray endovascular occlusion of the uterine arteries for ULM performed in 88 women aged 34-46 years (mean age 38.8 ± 2.5 years). The patients were divided into 2 groups: the 1st group comprised 65 patients without visible uterine-ovarian interarterial anastomoses. They performed standard embolization of the uterine arteries (EUA) using spherical PVA microemboli (COOK, USA), Embosphere (Merit Medical, USA) with a diameter of 500-700 microns. The second group consisted of 23 patients in whom utero-ovarian inter-arterial anastomoses were detected. In patients of this group, EUAs were produced with Embox cylindrical emboli (Plastis-M, Russia) with a length of 10 mm and a diameter of 500-700 μm, which occlude only the bed of the uterine arteries and are not capable of to overcome utero-ovarian inter-arterial anastomoses. In the 2nd group of EUA patients wore the character of occlusion, separating the uterine and ovarian arteries. The original EUA protocol was applied, which includes, in addition to the standard stages of selective arteriography of the uterine arteries, performing preliminary abdominal aortography to visualize the ovarian arteries and pelvic arteriography to assess pelvic vascular anatomy and identify utero-ovarian interarterial anastomoses. The results of the study. A total angiographic examination of the ovarian and uterine arteries, including a review angiography of the infrarenal section and bifurcation of the aorta, ileal vessels. In 23 (26.1%) patients with angiographic examination, uterine-ovarian arterio-arterial anastomoses. In 13 patients (56.5% of the detected anastomoses), these were type 1 anastomoses. In 10 patients (43.5% of the detected anastomoses), type 3 anastomoses were detected. Endovascular occlusion of the uterine arteries was performed in all patients. In 5 (7.69%) patients from the 1st group after EUA, amenorrhea occurred. In contrast, in all 23 patients from the 2nd group in the postembolization period, no observation of ovarian function was observed in any of the observations. Conclusion. For endovascular treatment of ULM in the presence of pronounced utero-ovarian interarterial anastomoses, the method of separating uterine artery occlusion is a safe and effective way to prevent ischemic damage to the ovaries.
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Cúneo, Nicasio, Alejandro Soderini, Lucía Rodich, Carlos Reyes, Claudia Arias, Alejandro Aragona, and Evangelina Bonavía. "Traquelectomía radical abdominal con preservación de la arteria uterina (TRAPAU ): presentación de la técnica quirúrgica y evaluación de resultados iniciales." Revista Peruana de Ginecología y Obstetricia 55, no. 4 (April 28, 2015): 273–80. http://dx.doi.org/10.31403/rpgo.v55i304.
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Objetivos: Presentar una variante técnica de la traquelectomía radical abdominal, preservando la integridad de ambas arterias uterinas (TRAPAU); su factibilidad y resultados iniciales. Diseño: Estudio clínico quirúrgico. Institución: Hospital Oncológico de Buenos Aires Marie Curie, Argentina. Participantes: Mujeres con cáncer de cérvix uterino estadios Ia2 – Ib1. Intervenciones: Se presenta una técnica diseñada para el tratamiento conservador de la fertilidad, para pacientes con cáncer de cérvix uterino estadios Ia2 – Ib1. Nueve pacientes con edad promedio 28,5 años (20 a 32 años) y tumor central clínico <2 cm fueron tratadas entre octubre 2004 y octubre 2008. Las pacientes fueron estatificadas según criterios FIGO, previo consentimiento informado. La técnica quirúrgica consistió en: 1) laparotomía exploradora con disección de fosas, espacios y linfadenectomía pélvica bilateral, con biopsia por congelación de los ganglios; 2) disección de la arteria uterina desde su nacimiento; 3) disección del uréter en todo su trayecto; 4) sección de parametrios anteriores, posteriores y laterales, preservando el nervio y plexo hipogástricos; 5) diéresis de mango vaginal en 2 colgajos, anterior y posterior; 6) sección del cérvix a nivel ístmicocervical, con biopsia introperatoria del margen superior del cuello uterino; 7) síntesis vaginal al istmo. Principales medidas de resultados: Factibilidad quirúrgica, pérdida sanguínea, tiempo operatorio, complicaciones, duración de internación, radicalidad quirúrgica por estudio anatomopatológico de la pieza operatoria, gestaciones y recidivas. Resultados: La técnica pudo realizarse satisfactoriamente en todos los casos. En dos, se completó con la histerectomía, debido a márgenes cervicales comprometidos. Duración 180 minutos. Débito sanguíneo 600 mL. Fueron complicaciones un caso de dispareunia más poliposis cervical y un caso de dismenorrea. En el seguimiento de 2 a 50 meses, se verificó una gestación y una recidiva central. Conclusiones: La TRAPAU ha demostrado ser quirúrgicamente factible, con óptima radicalidad quirúrgica, manteniendo la integridad de la irrigación uterina, lo que preserva mejor la funcionalidad del aparato reproductor.
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Kabine, M., H. Chraibi-Kaadoud, A. Bassir, H. Jalal, H. Asmouki, A. Aboulfalah, and A. Soummani. "FAUX ANEVRYSME DE L ARTERE UTERINE : ETIOLOGIE INHABITUELLE DES HEMORRAGIES DU POST-PARTUM." International Journal of Advanced Research 10, no. 04 (April 30, 2022): 979–84. http://dx.doi.org/10.21474/ijar01/14633.
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Le faux anevrysme de lartere uterine est une complication rare, encore mal connue de la cesarienne, il est responsable dune hemorragie du post-partum secondaire, le plus souvent severe. Nous rapportons une observation dun faux anevrysme de lartere uterine gauche survenu 1 mois apres accouchement par cesarienne et revele par des metrorragies. Le diagnostic repose sur les donnees echographiques couple au Doppler vasculaire.Langiographie des arteres uterines constitue lexamen de reference. Son rôle est double, diagnostique et therapeutique par embolisation arterielle selective permettant lexclusion definitive de la lesion, tout en preservant la fertilite des patientes. Summary: The false aneurysm of the uterine artery is a rare, still poorly understood complication of caesarean section, it is an uncommun cause of secondary postpartum hemorrhage, most often severe. We report a case of a false aneurysm of the left uterine artery which occurred 1 month after caesarean delivery, revealed by metrorrhagia. Diagnosis is based on ultrasound data coupled with vascular Doppler. Angiography of the uterine arteries is the reference examination. Its role is twofold: diagnostic and therapeutic by selective arterial embolization allowing the definitive exclusion of the lesion, while preserving the fertility of the patients.
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Lin, Chen, Hong He, Ning Cui, Zongli Ren, Minglin Zhu, and Raouf A. Khalil. "Decreased uterine vascularization and uterine arterial expansive remodeling with reduced matrix metalloproteinase-2 and -9 in hypertensive pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 1 (January 1, 2020): H165—H180. http://dx.doi.org/10.1152/ajpheart.00602.2019.
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Normal pregnancy involves extensive remodeling of uterine and spiral arteries and matrix metalloproteinases (MMPs)-mediated proteolysis of extracellular matrix (ECM). Preeclampsia is characterized by hypertension in pregnancy (HTN-Preg) and intrauterine growth restriction (IUGR) with unclear mechanisms. Initial faulty placentation and reduced uterine perfusion pressure (RUPP) could release cytoactive factors and trigger an incessant cycle of suppressed trophoblast invasion of spiral arteries, further RUPP, and progressive placental ischemia leading to HTN-Preg and IUGR; however, the extent and depth of uterine vascularization and the proteolytic enzymes and ECM proteins involved are unclear. We hypothesized that HTN-Preg involves decreased uterine vascularization and arterial remodeling by MMPs and accumulation of ECM collagen. Blood pressure (BP) and fetal parameters were measured in normal Preg rats and RUPP rat model, and the uteri were assessed for vascularity, MMP levels, and collagen deposition. On gestational day 19, BP was higher, and the uterus weight, litter size, and pup weight were reduced in RUPP vs. Preg rats. Histology of uterine tissue sections showed reduced number (5.75 ± 0.95 vs. 11.50 ± 0.87) and size (0.05 ± 0.01 vs. 0.12 ± 0.02 mm2) of uterine spiral arterioles in RUPP vs. Preg rats. Immunohistochemistry showed localization of endothelial cell marker cluster of differentiation 31 (CD31) and smooth muscle marker α-actin in uterine arteriolar wall and confirmed decreased number/size of uterine arterioles in RUPP rats. The cytotrophoblast marker cytokeratin-7 showed less staining and invasion of spiral arteries in the deep decidua of RUPP vs. Preg rats. Uterine arteries showed less expansion in response to increases in intraluminal pressure in RUPP vs. Preg rats. Western blot analysis, gelatin zymography, and immunohistochemistry showed decreases in MMP-2 and MMP-9 and increases in the MMP substrate collagen-IV in uterus and uterine arteries of RUPP vs. those in Preg rats. The results suggest decreased number, size and expansiveness of spiral and uterine arteries with decreased MMP-2 and MMP-9 and increased collagen-IV in HTN-Preg. Decreased uterine vascularization and uterine arterial expansive remodeling by MMPs could be contributing mechanisms to uteroplacental ischemia in HTN-Preg and preeclampsia. NEW & NOTEWORTHY Preeclampsia is a pregnancy-related disorder in which initial inadequate placentation and RUPP cause the release of cytoactive factors and trigger a ceaseless cycle of suppressed trophoblast invasion of spiral arteries, further RUPP, and progressive placental ischemia leading to HTN-Preg and IUGR; however, the extent/depth of uterine vascularization and the driving proteolytic enzymes and ECM proteins are unclear. This study shows decreased number, size, and expansiveness of uterine spiral arteries, with decreased MMP-2 and MMP-9 and increased collagen-IV in HTN-Preg rats. The decreased uterine vascularization and uterine arterial expansive remodeling by MMPs could contribute to progressive uteroplacental ischemia in HTN-Preg and preeclampsia.
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Weiner, C., K. Z. Liu, L. Thompson, J. Herrig, and D. Chestnut. "Effect of pregnancy on endothelium and smooth muscle: their role in reduced adrenergic sensitivity." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1275—H1283. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1275.
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During pregnancy, vascular reactivity of the uterine artery is characterized by decreased contraction to norepinephrine and increased relaxation to acetylcholine. We investigated whether 1) relaxation to A23187 is increased during pregnancy and 2) endothelium-derived relaxing factor (EDRF) and/or prostaglandins are responsible for the decreased uterine artery sensitivity to norepinephrine during pregnancy. Isolated rings of uterine and carotid arteries were obtained from pregnant and nonpregnant guinea pigs. Relaxation to sodium nitroprusside in uterine but not carotid artery was reduced during pregnancy. Relaxation of both uterine and carotid arteries to the calcium ionophore A23187 was unaffected by pregnancy. During pregnancy, contractions to norepinephrine were reduced in the uterine artery compared with arteries from nonpregnant animals. Indomethacin slightly enhanced the contractions of uterine artery to norepinephrine during pregnancy. However, indomethacin-treated uterine arteries from pregnant animals were still less responsive to norepinephrine than control uterine arteries from nonpregnant animals. Methylene blue enhanced the efficacy of norepinephrine in uterine arteries of nonpregnant animals as well as carotid arteries of pregnant and nonpregnant animals but not in uterine arteries of pregnant animals. In contrast, N-monomethyl-L-arginine, a specific inhibitor of EDRF synthesis, not only enhanced uterine and carotid artery responses to norepinephrine in both pregnant and nonpregnant animals but fully reversed the blunted potency of norepinephrine on uterine arteries of pregnant to that of nonpregnant animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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Xiao, DaLiao, XiaoHui Huang, Soochan Bae, Charles A. Ducsay, Lawrence D. Longo, and Lubo Zhang. "Cortisol-mediated regulation of uterine artery contractility: effect of chronic hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 2 (February 2004): H716—H722. http://dx.doi.org/10.1152/ajpheart.00805.2003.
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We previously demonstrated that cortisol regulated α1-adrenoceptor-mediated contractions differentially in nonpregnant and pregnant uterine arteries. Given that chronic hypoxia during pregnancy has profound effects on maternal uterine artery reactivity, the present study investigated the effects of chronic hypoxia on cortisol-mediated regulation of uterine artery contractions. Pregnant ( day 30) and nonpregnant ewes were divided between normoxic control and chronically hypoxic [maintained at high altitude (3,820 m), arterial Po2: 60 mmHg for 110 days] groups. Uterine arteries were isolated and contractions measured. In hypoxic animals, cortisol (10 ng/ml for 24 h) increased norepinephrine-induced contractions in pregnant, but not in nonpregnant, uterine arteries. The 11β-hydroxysteroid dehydrogenase inhibitor carbenoxolone did not change cortisol effects in nonpregnant uterine arteries, but abolished it in pregnant uterine arteries by increasing norepinephrine pD2 (–log EC50) in control tissues. The dissociation constant of norepinephrine-α1-adrenoceptors was not changed by cortisol in nonpregnant, but decreased in pregnant uterine arteries. There were no differences in the density of glucocorticoid receptors between normoxic and hypoxic tissues. Cortisol inhibited the norepinephrine-induced increase in Ca2+ concentrations in nonpregnant arteries, but potentiated it in pregnant arteries. In addition, cortisol attenuated phorbol 12,13-dibutyrate-induced contractions in normoxic nonpregnant and pregnant uterine arteries, but had no effect on the contractions in hypoxic arteries. The results suggest that cortisol differentially regulates α1-adrenoceptor- and PKC-mediated contractions in uterine arteries. Chronic hypoxia suppresses uterine artery sensitivity to cortisol, which may play an important role in the adaptation of uterine vascular tone and blood flow in response to chronic stress of hypoxia during pregnancy.
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Idowu, Bukunmi, Bolanle Ibitoye, and Victor Adetiloye. "Uterine Artery Doppler Velocimetry of Uterine Leiomyomas in Nigerian Women." Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics 39, no. 09 (August 7, 2017): 464–70. http://dx.doi.org/10.1055/s-0037-1604489.
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Objective To describe the blood flow velocities and impedance indices changes in the uterine arteries of leiomyomatous uteri using Doppler sonography. Methods This was a prospective, case-control study conducted on 140 premenopausal women with sonographic diagnosis of uterine leiomyoma and 140 premenopausal controls without leiomyomas. Pelvic sonography was performed to diagnose and characterize the leiomyomas. The hemodynamics of the ascending branches of both main uterine arteries was assessed by Doppler interrogation. Statistical analysis was performed mainly using non-parametric tests. Results The median uterine volume of the subjects was 556 cm3, while that of the controls was 90.5 cm3 (p < 0.001). The mean peak systolic velocity (PSV), end-diastolic velocity (EDV), time-averaged maximum velocity (TAMX), time-averaged mean velocity (Tmean), acceleration time (AT), acceleration index (AI), diastolic/systolic ratio (DSR), diastolic average ratio (DAR), and inverse pulsatility index (PI) were significantly higher in the subjects (94.2 cm/s, 29.7 cm/s, 49.1 cm/s, 25.5 cm/s, 118 ms, 0.8, 0.3, 0.6, and 0.8 respectively) compared with the controls (54.2 cm/s, 7.7 cm/s, 20.0 cm/s, 10.0 cm/s, 92.0 ms, 0.6, 0.1, 0.4, and 0.4 respectively); p < 0.001 for all values. Conversely, the mean PI, resistivity index (RI), systolic/diastolic ratio (SDR) and impedance index (ImI) of the subjects (1.52, 0.70, 3.81, and 3.81 respectively) were significantly lower than those of the controls (2.38, 0.86, 7.23, and 7.24 respectively); p < 0.001 for all values. Conclusion There is a significantly increased perfusion of leiomyomatous uteri that is most likely due to uterine enlargement.
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Xiao, DaLiao, and Lubo Zhang. "Adaptation of uterine artery thick- and thin-filament regulatory pathways to pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 1 (January 2005): H142—H148. http://dx.doi.org/10.1152/ajpheart.00655.2004.
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Little is known about the adaptation of uterine artery smooth muscle contractile mechanisms to pregnancy. The present study tested the hypothesis that pregnancy differentially regulates thick- and thin-filament regulatory pathways in uterine arteries. Isometric tension, intracellular free Ca2+ concentration, and phosphorylation of 20-kDa myosin light chain (MLC20) were measured simultaneously in uterine arteries isolated from nonpregnant and near-term (140 days gestation) pregnant sheep. Phenylephrine-mediated intracellular free Ca2+ concentration, MLC20 phosphorylation, and contraction tension were significantly increased in uterine arteries of pregnant compared with nonpregnant animals. In contrast, phenylephrine-mediated Ca2+ sensitivity of MLC20 phosphorylation was decreased in the uterine arteries of pregnant sheep. Simultaneous measurement of phenylephrine-stimulated tension and MLC20 phosphorylation in the same tissue indicated a decrease in MLC20 phosphorylation-independent contractions in the uterine arteries of pregnant sheep. In addition, activation of PKC produced significantly lower sustained contractions in uterine arteries of pregnant compared with nonpregnant animals in the absence of changes in MLC20 phosphorylation levels in either vessels. In uterine arteries of nonpregnant sheep, the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase inhibitor PD-098059 significantly increased phenylephrine-mediated, MLC20 phosphorylation-independent contractions. The results suggest that in uterine arteries, pregnancy upregulates α1-adrenoceptor-mediated Ca2+ mobilization and MLC20 phosphorylation. In contrast, pregnancy downregulates the Ca2+ sensitivity of myofilaments, which is mediated by both thick- and thin-filament pathways.
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Apaza Valencia, John, and Juan Delgado Rendón. "Índices y velocidades de la arteria uterina como indicadores de hipoperfusión uterina en gestantes con restricción del crecimiento intrauterino." Revista Peruana de Ginecología y Obstetricia 61, no. 4 (January 16, 2016): 355–61. http://dx.doi.org/10.31403/rpgo.v61i1865.
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Objetivo: Evaluar los índices y velocidades de la arteria uterina como indicadores de hipoperfusión uterina en gestantes con restricción del crecimiento intrauterino. Diseño: Estudio analítico, de casos y controles. Institución: Hospital III Honorio Delgado de Arequipa, Perú. Participantes: Treinta gestantes con restricción del crecimiento intrauterino (RCIU) con peso del recién nacido menor al percentil 10; el grupo control estuvo conformado por 80 gestantes normales en el tercer trimestre. Metodología: Entre julio del 2013 y abril del 2014 se realizó ecografía Doppler de las arterias uterinas en las gestantes que participaron del estudio, se calculó los índices y velocidades de las arterias uterinas, se comparó las medias y se hizo pruebas de validez diagnóstica de RCIU. Principales medidas de resultados: Índices y velocidades de las arterias uterinas. Resultados: La media de la edad gestacional para los grupos de RCIU y control fueron 35,7 y 36,2 semanas, respectivamente. La media del peso de los RN con RCIU fue 1 932,60 g. La velocidad media (MnV) presentó sensibilidad 73%, especificidad 95%, valor predictivo positivo (VPP) 85%, valor predictivo negativo (VPN) 90%, odds ratio (OR) 52 y razón de verosimilitud de 14,6. Los índices de pulsatilidad (IP) y de resistencia (IR) mostraron sensibilidad de 27%, especificidad 95%, VPP 67%, VPN 78%, OR 6,9 y razón de verosimilitud 5,3. Conclusiones: Las velocidades y especialmente la velocidad media de la arteria uterina tuvieron mejor sensibilidad, VPP, VNP, OR y razón de verosimilitud que los índices, como indicadores de hipoperfusión uterina en gestantes con restricción del crecimiento intrauterino.
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Xiao, Daliao, and Lubo Zhang. "ERK MAP kinases regulate smooth muscle contraction in ovine uterine artery: effect of pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 1 (January 1, 2002): H292—H300. http://dx.doi.org/10.1152/ajpheart.2002.282.1.h292.
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The present study investigated the potential role of extracellular signal-regulated kinase (ERK) in uterine artery contraction and tested the hypothesis that pregnancy upregulated ERK-mediated function in the uterine artery. Isometric tension in response to phenylephrine (PE), serotonin (5-HT), phorbol 12,13-dibutyrate (PDBu), and KCl was measured in the ring preparation of uterine arteries obtained from nonpregnant and near-term (140 days gestation) pregnant sheep. Inhibiting ERK activation with PD-98059 did not change the KCl-evoked contraction but significantly inhibited the contraction to 5-HT in both nonpregnant and pregnant uterine arteries. PD-98059 did not affect PE-induced contraction in the uterine arteries of nonpregnant sheep but significantly decreased it in the uterine arteries of pregnant sheep. In accordance, PE stimulated activation of ERK in uterine arteries of pregnant sheep, which was blocked by PD-98059. PD-98059-mediated inhibition of the PE-induced contraction was associated with a decrease in both intracellular Ca2+ concentration and Ca2+ sensitivity of contractile proteins in the uterine arteries of pregnant sheep. PDBu-mediated contraction was significantly less in pregnant than in nonpregnant uterine arteries. PD-98059 had no effect on PDBu-induced contraction in nonpregnant but significantly increased it in pregnant uterine arteries. In addition, PD-98059 significantly enhanced PDBu-stimulated protein kinase C activity. The results indicate that ERK plays an important role in the regulation of uterine artery contractility, and its effect is agonist dependent. More importantly, pregnancy selectively enhances the role of ERK in α1-adrenoceptor-mediated contractions and its effect in suppressing protein kinase C-mediated contraction in the uterine artery.
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Daye, М. М., D. A. Niauri, V. К. Ryjkov, and I. V. Sergeeva. "The evaluation of uterine arteries embolization value in functional surgery in patients with uterine myoma." Journal of obstetrics and women's diseases 54, no. 3 (November 1, 2005): 45–49. http://dx.doi.org/10.17816/jowd83454.
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The experience of constant embolization of uterine arteries (60 patients) has shown that constant intravascular occlusion of uterine arteries in some cases may be considered as rational intervention and an alternative for organ-saved surgery. Temporary embolization of uterine arteries (20 patients) orientated to decreasing of intraoperative bleeding risk allows to perform reconstructive-plastic uterine surgery in optimal condititons.
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NADERALI, Ebrahim K., Patrick J. DOYLE, and Gareth WILLIAMS. "Resveratrol induces vasorelaxation of mesenteric and uterine arteries from female guinea-pigs." Clinical Science 98, no. 5 (April 3, 2000): 537–43. http://dx.doi.org/10.1042/cs0980537.
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Naturally occurring hydroxystilbenes have been shown to induce vasorelaxation. Here, we studied the mechanism of resveratrol-induced vasorelaxation in different types of blood vessels, namely mesenteric (resistance) and main uterine (conductance) arteries, from female guinea-pigs on day 7 and day 15 of the oestrous cycle. Resveratrol (5–70 µmol/l) induced concentration-dependent relaxation of both mesenteric and uterine arteries preconstricted with either noradrenaline (NA; 10 µmol/l) or KCl (125 mmol/l). Resveratrol was 2-fold more potent in inducing relaxation of mesenteric arteries than of uterine arteries. Its effects on uterine arteries from both day-7 and day-15 guinea-pigs were similar, irrespective of the constrictor used, but it was significantly (P < 0.01) more potent in inducing relaxation of mesenteric arteries contracted with NA compared with those constricted with KCl. In day-7 arteries precontracted with NA, NG-nitro-l-arginine methyl ester (l-NAME; 10 µmol/l) had no effects on the time course of resveratrol-induced vasorelaxation in either mesenteric or uterine arteries. However, indomethacin (50 µmol/l) significantly (P < 0.05) potentiated resveratrol's effect on mesenteric, but not uterine, arteries. Indomethacin had no effect on resveratrol-induced vasorelaxation of arteries contracted with KCl, whereas l-NAME significantly (P < 0.05) reduced the effects of resveratrol on uterine, but not on mesenteric, arteries. In day-15 arteries, l-NAME significantly (P < 0.01) attenuated the effects of resveratrol on mesenteric arteries contracted with NA. Indomethacin had no effect on resveratrol activity. This study indicates that: (a) the effect of resveratrol on resistance arteries is greater than that on conductance arteries; (b) the effects of resveratrol are not mediated via prostanoids, but NO may play a role; and (c) the stage of the oestrous cycle has no influence on resveratrol-induced vasorelaxation.
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MARTÍNEZ-CABRERA, LESLIE, and JORGE YBASETA-MEDINA. "ÍNDICE DE PULSATILIDAD DE LA ARTERIA UTERINA ENTRE LAS 11 Y 14 SEMANAS DE GESTACIÓN, COMO PREDICTOR DE PREECLAMPSIA." Revista Médica Panacea 9, no. 2 (August 29, 2020): 124–29. http://dx.doi.org/10.35563/rmp.v9i2.332.
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Introducción: El índice de pulsatilidad de la arteria uterina puede usarse para estimar el riesgo de preeclampsia. En el segundo y tercer trimestre del embarazo. Objetivo: Generar conocimiento sobre el índice de pulsatilidad de las arterias uterinas en la predicción de la preeclampsia en gestantes entre 11 y 14 semanas. Materiales y métodos: Es un estudio descriptivo de búsqueda bibliografía y se ha realizado en Pubmed, Medline, Scielo, bibliotecas de universidades nacionales e internacionales. Resultados: La media del índice de pulsatilidad en las gestantes con preeclampsia encontrado fue variada que va de 1.92 a 2.41, teniendo como puntos de corte de IP > 1.71 (p<0,05), en el doppler color de la arteria uterina a las 11-14 semanas de gestación. La asociación de pre-eclampsia según el índice de pulsatilidad de la arteria uterina entre las 11 y 14 semanas, es un buen método para el cribado de mujeres en riesgo de desarrollar preeclampsia, ya que presenta una sensibilidad, especificidad, VPP y VPN variada, pero suficiente para aceptarlo como método predictor de pre-eclampsia. Conclusiones: Existe suficiente evidencia que concluye que el uso del índice de pulsatilidad por ecografía doppler de la arteria uterina es un método adecuado para la detección a las 11 a 14 semanas de gestación en mujeres para desarrollar pre-eclampsia. Palabras clave: Preeclampsia, Efecto Doppler; Gestación (fuente: DeCS BIREME)><0,05), en el doppler color de la arteria uterina entre las 11 y 14 semanas, es un buen método para el cribado de las mujeres en riesgo de desarrollar preclampsia, ya que presenta una sensibilidad, especificidad, VPP y VPN variada, pero suficiente para aceptarlo como método predictor de pre-eclampsia. Conclusión: Existe suficiente evidencia que concluye que el uso del índice de pulsatilidad por ecografía doppler de la arteria uterina es un método adecuado para la detección a las 11 a 14 semanas de gestación en mujeres para desarrollar pre-eclampsia.
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Gupta, Sumiti, Renuka Verma, and Rajnish Kalra. "Uterine Arterio-Venous Malformation: A Rare Post Mortem Finding in a Young Female." International Journal of Health Sciences and Research 11, no. 11 (November 11, 2021): 130–33. http://dx.doi.org/10.52403/ijhsr.20211116.
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Uterine arterio-venous malformation is one of the differentials of dysfunctional uterine bleeding that can result in life-threatening emergency with sudden, unexpected massive vaginal bleeding. We describe a case of 20-year old female, who presented with sudden heavy vaginal bleeding and was diagnosed with uterine arterio-venous malformation on post-mortem examination. High index of suspicion is required to make a timely diagnosis for appropriate management and to avoid maternal morbidity and mortality. Key words: Uterine arterio-venous malformations, embolization, dysfunctional uterine bleeding.
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Vodstrcil, L. A., J. Novak, M. Tare, M. E. Wlodek, and L. J. Parry. "221. Localisation of relaxin receptors (Rxfp1) in the uterine artery and the effects of blocking circulating relaxin on passive mechanical wall properties in the uterine artery of late pregnant rats." Reproduction, Fertility and Development 20, no. 9 (2008): 21. http://dx.doi.org/10.1071/srb08abs221.
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During pregnancy, the uteroplacental circulation undergoes dramatic alterations to allow for the large increase in blood flow to the feto-placental unit. These alterations are achieved through several mechanisms including structural changes in the uterine artery wall and endothelium-dependent vasodilation. Small renal arteries of relaxin-deficient mice and rats have enhanced myogenic reactivity and decreased passive compliance, and are relatively vasoconstricted (Novak et al. 2001, 2006). To date, no study has identified relaxin receptors (Rxfp1) in arteries or investigated the effects of relaxin deficiency in pregnancy on uterine artery function. The aims of this current study were to: 1) localise Rxfp1 in the uterine arteries, 2) measure myogenic reactivity in small uterine arteries after relaxin treatment, and 3) test the hypothesis that blocking circulating relaxin in late pregnancy will increase uterine artery wall stiffness. We demonstrated that Rxfp1 is expressed in the uterine arteries of pregnant mice and rats. Brightfield immunohistochemistry and immunofluorescence using antibodies specific for rat Rxfp1, α-smooth muscle actin and CD31 localised Rxfp1 protein predominantly to the vascular smooth muscle in the uterine artery of pregnant rats. Administration of recombinant human H2 relaxin (4 ug/h) for 6 h or 5 days in intact and ovariectomised rats reduced myogenic reactivity of small uterine arteries in vitro. Pregnant rats were treated with a monoclonal antibody against circulating relaxin (MCA1) or control (MCAF) for 3 days (Days 17–19) and uterine arteries were mounted on a pressure myograph to assess passive mechanical wall properties. Neutralising circulating relaxin in late pregnancy resulted in a significant increase in uterine artery wall stiffness. These data demonstrate that relaxin acts on the vascular smooth muscle cells in the uterine artery and may be involved in the pregnancy-specific vascular remodelling of uterine arteries to increase vasodilation and blood flow to the uterus and placenta. (1) Novak J et al. (2001). J Clin Invest 107: 1469–75 (2) Novak J et al. (2006). FASEB J 20: 2352–62
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Kim, Jeong-Eun, Young Ho So, Byoung Jae Kim, Sun Min Kim, Young Ho Choi, and Chang Kyu Sung. "Postpartum hemorrhage from non-uterine arteries: clinical importance of their detection and the results of selective embolization." Acta Radiologica 59, no. 8 (October 24, 2017): 932–38. http://dx.doi.org/10.1177/0284185117738547.
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Background Identification of the source of postpartum hemorrhage (PPH) is important for embolization because PPH frequently originates from non-uterine arteries. Purpose To evaluate the clinical importance of identifying the non-uterine arteries causing the PPH and the results of their selective embolization. Material and Methods This retrospective study enrolled 59 patients who underwent embolization for PPH from June 2009 to July 2016. Angiographic findings and medical records were reviewed to determine whether non-uterine arteries contributed to PPH. Arteries showing extravasation or hypertrophy accompanying uterine hypervascular staining were regarded as sources of the PPH. The results of their embolization were analyzed. Results Of 59 patients, 19 (32.2%) underwent embolization of non-uterine arteries. These arteries were ovarian (n = 7), vaginal (n = 5), round ligament (n = 5), inferior epigastric (n = 3), cervical (n = 2), internal pudendal (n = 2), vesical (n = 1), and rectal (n = 1) arteries. The embolic materials used included n-butyl cyanoacrylate (n = 9), gelatin sponge particles (n = 8), gelatin sponge particles with microcoils (n = 1), and polyvinyl alcohol particles (n = 1). In 13 patients, bilateral uterine arterial embolization was performed. Re-embolization was performed in two patients with persistent bleeding. Hemostasis was achieved in 17 (89.5%) patients. Two patients underwent immediate hysterectomy due to persistent bleeding. One patient experienced a major complication due to pelvic organ ischemia. One patient underwent delayed hysterectomy for uterine infarction four months later. Conclusion Non-uterine arteries are major sources of PPH. Detection and selective embolization are important for successful hemostasis.
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Ni, Y., V. May, K. Braas, and G. Osol. "Pregnancy augments uteroplacental vascular endothelial growth factor gene expression and vasodilator effects." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (August 1, 1997): H938—H944. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h938.
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This study examined a potential role for vascular endothelial growth factor (VEGF) in uterine artery remodeling and vasodilation during pregnancy. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect VEGF mRNA in uterine tissues from nonpregnant (NP), midpregnant (MP, 15-16 days), and late-pregnant (LP, 19-21 days) rats and in placentas from MP and LP rats. VEGF mRNA levels in uteri and placentas were determined by Northern blotting, and the vasorelaxant activity of recombinant human VEGF (rh-VEGF) was tested and compared in isolated uterine arteries from LP and NP animals. VEGF120 and VEGF164 were the major isoforms detected in uterine tissues; all members of the VEGF family (VEGF120, VEGF164, VEGF188, and VEGF205) were expressed in LP placentas. VEGF mRNA levels increased 60% in MP and 80% in LP above those in NP (P < 0.05) in uterine tissues; VEGF mRNA levels were also detectable in placentas and elevated approximately fivefold in LP vs. MP tissues (P < 0.01). Phenylephrine-preconstricted uterine arcuate arteries (NP and LP) dilated in response to rhVEGF, an effect that was completely abolished by endothelial denudation or pretreatment with genistein, a tyrosine kinase inhibitor. The magnitude of dilation to an intermediate concentration of rhVEGF (1 nM) was greater in LP than in NP vessels (55 +/- 8 vs. 24 +/- 11%; P < 0.05), and this effect was diminished comparably in both groups (approximately 60% by N omega-nitro-L-arginine, an inhibitor of nitric oxide synthesis. These results suggest that VEGF may play a role in the vascular remodeling and vasodilation that lead to decreased uterine vascular resistance and increased uterine blood flow during pregnancy.
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Xiao, Daliao, William J. Pearce, and Lubo Zhang. "Pregnancy enhances endothelium-dependent relaxation of ovine uterine artery: role of NO and intracellular Ca2+." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (July 1, 2001): H183—H190. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h183.
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The present study tested the hypothesis that the pregnancy-associated increase in endothelium-dependent relaxation of the uterine artery was mediated primarily by an increase in nitric oxide (NO) release, resulting in a reduction in smooth muscle intracellular Ca2+ concentration ([Ca2+]i). Uterine arteries obtained from nonpregnant and near-term (140 days gestation) pregnant sheep were used. The Ca2+ ionophore A23187 induced endothelium-dependent relaxations in both nonpregnant and pregnant uterine arteries, with an increased relaxation in the pregnant tissue. In contrast, endothelium-independent relaxations induced by sodium nitroprusside were the same in nonpregnant and pregnant arteries. In addition, removal of the endothelium significantly increased noradrenaline-induced contractions in pregnant, but not nonpregnant, uterine arteries. In accordance, pregnancy increased both basal and A23187 -stimulated NO releases in the uterine artery. Simultaneous measurement of tension and [Ca2+]i in the smooth muscle demonstrated a linear correlation with the slope of unity between A23187 -induced relaxation and the reduction of [Ca2+]i in both nonpregnant and pregnant uterine arteries. The A23187 -induced reduction of [Ca2+]i was significantly enhanced in pregnant, compared with nonpregnant, uterine arteries. The results indicate that pregnancy increases NO release, which, through decreasing [Ca2+]i in the smooth muscle, accounts for the increased endothelium-dependent relaxation of the uterine artery. Signal transduction pathways distal to NO production are not changed by pregnancy.
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Boone, Christine, Yilun Koethe, Maureen Kohi, and Evan Lehrman. "Collateral Uterine Arterial Supply in the Setting of Various Uterine Pathologies." Journal of Clinical Interventional Radiology ISVIR 02, no. 03 (December 2018): 191–96. http://dx.doi.org/10.1055/s-0038-1676166.
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AbstractIn most patients, bilateral uterine arteries supply the uterus exclusively. However, collateral arterial supply to the uterus has been described, predominantly in the context of uterine artery embolization (UAE) for fibroid treatment. This may lead to incomplete embolization, which can impact clinical outcomes. Therefore, identification of potential collateral supply to the uterus is essential for achieving optimal clinical results. The authors report three cases of collateral uterine arterial supply from the ovarian and round ligament arteries in the setting of uterine arteriovenous fistula (uAVF), postpartum hemorrhage (PPH), and symptomatic fibroids. Aortography from the level of the renal arteries was performed for initial evaluation of uterine arterial supply in all patients and identified hypertrophied, tortuous ovarian artery collaterals. Selective angiography of the external iliac artery was required to identify round ligament collateral uterine supply. Three-dimensional cone beam computed tomography (CT) was also used to visualize vascular distribution of bilateral uterine arteries and an ovarian collateral feeding a uAVF. In regard to outcomes, identification of collateral uterine arterial supply allowed for single-session complete embolization in fibroid patients with collateralized round ligament or ovarian arteries and in the PPH patient in disseminated intravascular coagulation with predominantly ovarian artery supply to the uterus. Identification of collateral uterine arterial supply facilitated technical success in all patients. In the setting of various uterine pathologies, identification of collateral uterine arterial supply is essential to optimize clinical success of UAE.
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Xiao, Daliao, Xiaohui Huang, Lawrence D. Longo, William J. Pearce, and Lubo Zhang. "Regulation of baseline Ca2+ sensitivity in permeabilized uterine arteries: effect of pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 1 (July 2006): H413—H420. http://dx.doi.org/10.1152/ajpheart.00103.2006.
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The adaptation of contractile mechanisms of the uterine artery to pregnancy is not fully understood. The present study examined the effect of pregnancy on the uterine artery baseline Ca2+ sensitivity. In β-escin-permeabilized arterial preparations, Ca2+-induced concentration-dependent contractions were significantly decreased in uterine arteries from pregnant animals compared with those of nonpregnant animals. Time-course studies showed that Ca2+ increased phosphorylation of 20-kDa myosin light chain (MLC20), which preceded the tension development in vessels from both pregnant and nonpregnant animals. When compared with vessels from nonpregnant animals, there was a significant increase in the protein level of MLC20 and an accordance increase in the level of Ca2+-induced phosphorylated MLC20 (MLC20-P) in uterine arteries during pregnancy. Simultaneous measurements of MCL20-P levels and contractions stimulated with Ca2+ in the same tissues demonstrated a significant attenuation in the tension-to-MLC20-P ratio in uterine arteries during pregnancy. Activation of PKC with phorbol 12,13-dibutyrate (PDBu) potentiated Ca2+-induced contractions in uterine arteries from nonpregnant but not pregnant animals. Accordingly, inhibition of PKC attenuated Ca2+-induced contractions in uterine arteries from nonpregnant but not pregnant animals. PDBu produced contractions in the presence or absence of Ca2+ in the β-escin-permeabilized arteries, which were significantly decreased in uterine arteries from pregnant compared with nonpregnant animals. The results suggest that pregnancy upregulates the thick-filament regulatory pathway by increasing MLC20 phosphorylation but downregulates the thin-filament regulatory pathway by decreasing the contractile sensitivity of MLC20-P, resulting in attenuated baseline Ca2+ sensitivity in the uterine artery. In addition, PKC plays an important role in the regulation of basal Ca2+ sensitivity, which is downregulated during pregnancy.
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Dorez, Maxence, Jérôme Delotte, Sébastien Novellas, Patrick Chevallier, and André Bongain. "Uterine arterio-venous malformation." International Journal of Emergency Medicine 3, no. 4 (August 21, 2010): 505–6. http://dx.doi.org/10.1007/s12245-010-0219-3.
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Juneja, Sunil Kumar, Pooja Tandon, and Gagandeep Kaur. "Success of uterine artery embolization in the management of postabortal arteriovenous malformations." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 9, no. 3 (February 27, 2020): 981. http://dx.doi.org/10.18203/2320-1770.ijrcog20200860.
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Background: Uterine artery arteriovenous malformations are an abnormal and non-functional connection between the uterine arteries and veins. It may be congenital or acquired. AVM can cause heavy menstrual bleeding and may have an impact on infertility. Uterine artery embolization is an alternate method to hysterectomy preserving the menstrual and reproductive function. Objectives of this study was to diagnose Arterio-venous malformations after abortions in patients with heavy menstrual bleeding and treating these patients with UAE.Methods: The retrospective study of patients with postabortal arteriovenous malformations managed at Dayanand Medical College and Hospital, during January 2012 to December 2018 was done. Inclusion criteria for this study post abortal heavy menstrual bleeding patients in reproductive age group diagnosed to be having AV malformations on CT angiography. Exclusion criteria for this study were H/O AUB prior to abortion, patients with fibroids, PID, endometriosis, adenomyosis, genital tract malignancies. Patients who do not have AV malformations on CT angiography.Results: This is a retrospective seven years study between January 2012 to December 2018 during which we received 23 patients who developed arterio-venous fistula following an abortion. The patients had heavy menstrual bleeding. All the patients had taken some hormonal treatment before reporting to us. All these patients underwent CT angiography. After that they all were subjected to UAE. All these patients were followed up to 6 months where they showed improvement in the symptoms.Conclusions: Acquired AVM is rare disorder following an abortion or a caesarean section. Heavy menstrual bleeding is a common symptom often requiring hysterectomy but with the advent of uterine artery embolization by blocking the uterine artery we can conserve the uterus where a lady can have normal menstrual and reproductive functions.
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Annibale, D. J., C. R. Rosenfeld, and K. E. Kamm. "Alterations in vascular smooth muscle contractility during ovine pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (May 1, 1989): H1282—H1288. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1282.
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During pregnancy, sheep develop attenuated systemic and uterine vascular responsiveness to alpha-adrenergic stimulation. To determine whether this reflects altered vascular smooth muscle function, we studied the responsiveness of smooth muscle isolated from systemic and uterine arteries to KCl and phenylephrine. Uterine, renal, and carotid arteries were collected from nonpregnant, pregnant (131 +/- 2 days, +/- SD), and late postpartum (144 +/- 4 days) ewes; endothelium was removed and open rings were hung for measurement of isometric force. There were no differences in concentration-response relationships nor maximal stresses generated to phenylephrine between nonpregnant, pregnant, and late postpartum states for carotid or renal arteries. However, the 50% maximal concentration for phenylephrine of uterine arteries in the nonpregnant state (2.8 +/- 0.9 x 10(-6) M) was greater than the pregnant state (0.76 +/- 0.05 x 10(-6) M). Moreover, uterine arteries from pregnant sheep generated significantly more stress than those from nonpregnant sheep (2.2 +/- 0.23 vs. 0.73 +/- 0.23 x 10(6) dyn/cm2, P less than 0.01). The attenuated systemic and uterine vascular responses associated with pregnancy do not result from diminished adrenergic sensitivity or contractile capability of arterial smooth muscle. In contrast, there is increased stress-generating capacity of uterine arterial smooth muscle during pregnancy, which is reversed during the postpartum period.
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Hu, Xiang-Qun, Rui Song, Monica Romero, Chiranjib Dasgupta, Joseph Min, Daisy Hatcher, Daliao Xiao, Arlin Blood, Sean M. Wilson, and Lubo Zhang. "Gestational Hypoxia Inhibits Pregnancy-Induced Upregulation of Ca 2+ Sparks and Spontaneous Transient Outward Currents in Uterine Arteries Via Heightened Endoplasmic Reticulum/Oxidative Stress." Hypertension 76, no. 3 (September 2020): 930–42. http://dx.doi.org/10.1161/hypertensionaha.120.15235.
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Hypoxia during pregnancy profoundly affects uterine vascular adaptation and increases the risk of pregnancy complications, including preeclampsia and fetal intrauterine growth restriction. We recently demonstrated that increases in Ca 2+ sparks and spontaneous transient outward currents (STOCs) played an essential role in pregnancy-induced uterine vascular adaptation. In the present study, we hypothesize that gestational hypoxia suppresses Ca 2+ sparks/STOCs coupling leading to increased uterine vascular tone via enhanced endoplasmic reticulum (ER)/oxidative stress. Uterine arteries were obtained from nonpregnant and near-term pregnant sheep residing in low altitude or acclimatizing to high-altitude (3801 m) hypoxia for ≈110 days. High-altitude hypoxia suppressed pregnancy-induced upregulation of RyR1 and RyR2 (ryanodine receptor 1 and 2) protein abundance, Ca 2+ sparks, and STOCs in uterine arteries. Inhibition of Ca 2+ sparks/STOCs with the RyR inhibitor ryanodine significantly increased pressure-dependent myogenic tone in uterine arteries from low-altitude normoxic pregnant animals but not those from high-altitude hypoxic pregnant animals. Gestational hypoxia significantly increased ER/oxidative stress in uterine arteries. Of importance, the hypoxia-mediated suppression of Ca 2+ sparks/STOCs and increase in myogenic tone in uterine arteries of pregnant animals were reversed by inhibiting ER/oxidative stress. Of great interest, the impaired sex hormonal regulation of STOCs in high-altitude animals was annulled by scavenging reactive oxygen species but not by inhibiting ER stress. Together, the findings reveal the differential mechanisms of ER and oxidative stresses in suppressing Ca 2+ sparks/STOCs and increasing myogenic tone of uterine arteries in hypoxia during gestation, providing new insights into the understanding of pregnancy complications associated with hypoxia.
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D'Angelo, G., and G. Osol. "Regional variation in resistance artery diameter responses to alpha-adrenergic stimulation during pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 1 (January 1, 1993): H78—H85. http://dx.doi.org/10.1152/ajpheart.1993.264.1.h78.
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Whole animal pressor responses are blunted during pregnancy; yet, uterine arteries, paradoxically, become significantly more sensitive to the constrictor effects of phenylephrine (PE). The objectives herein were to investigate 1) the regional variation (uterine vs. mesenteric arteries) in dose-lumen diameter relationship to alpha-adrenergic stimulation during pregnancy, and 2) the selectivity of these sensitivity shifts for this pathway (PE vs. KCl). Lumen diameter was measured in isolated, pressurized (50 mmHg) arterial segments from age-matched virgin (nonpregnant; NP) and late pregnant (LP; days 19-20) Sprague-Dawley rats. Uterine arcuate vs. mesenteric arteries from NP rats were equally sensitive to either vasoconstrictor. Arcuate arteries from LP rats, however, were 4.5-fold more sensitive to PE (P < 0.01) compared with those from NP controls. Furthermore, diameter curves became superimposed at [PE] > or = 0.1 microM, even though initial diameter of arcuate arteries from LP rats was significantly larger (P < 0.001). Conversely, mesenteric arteries from LP rats were three-fold less sensitive to PE (P < 0.02), and the diameter curve displayed a corresponding parallel rightward shift. Pregnancy did not affect the sensitivity to KCl depolarization in either arcuate or mesenteric arteries. The percent reduction in lumen diameter to the maximum [KCl] was significantly decreased only in arcuate arteries from LP rats (P < 0.001). Thus, during pregnancy, divergent constrictor responses specific to alpha-adrenergic stimulation occur in resistance arteries from the uterine vs. splanchnic circulations. Consequently, concentrations of PE that are subthreshold in NP uterine arteries can elicit large changes in lumen diameter and thereby have a pronounced effect on uterine vascular resistance in the pregnant state.
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Goulopoulou, Styliani, Johanna L. Hannan, Takayuki Matsumoto, Adviye Ergul, and R. Clinton Webb. "Augmented dilation to nitric oxide in uterine arteries from rats with type 2 diabetes: implications for vascular adaptations to pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 4 (February 15, 2014): H610—H618. http://dx.doi.org/10.1152/ajpheart.00588.2013.
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Pre-existing diabetes increases the risk of maternal and fetal complications during pregnancy, which may be due to underlying maternal vascular dysfunction and impaired blood supply to the uteroplacental unit. Endothelial dysfunction and reduced vascular smooth muscle responsiveness to nitric oxide (NO) are common vascular impairments in type 2 diabetes (T2D). We hypothesized that uterine arteries from diabetic rats would have reduced vascular smooth muscle sensitivity to NO compared with nondiabetic rats due to impairment in the NO/soluble guanylate cyclase (sGC)/cGMP signaling pathway. Uterine arteries from pregnant Goto-Kakizaki (GK; model of T2D) and Wistar (nondiabetic) rats were studied in a wire myograph. GK nonpregnant uterine arteries had reduced responses to ACh and sodium nitroprusside (SNP) but increased responses to propylamine propylamine NONOate and greater sensitivity to sildenafil compared with Wistar nonpregnant arteries. In late pregnancy, Wistar rats had reduced uterine vascular smooth muscle responsiveness to SNP, but GK rats failed to show this adaptation and had reduced expression of sGC compared with the nonpregnant state. GK rats had a smaller litter size (13.9 ± 0.48 vs. 9.8 ± 0.75; P < 0.05) and a greater number of resorptions compared with Wistar controls (0.8 ± 0.76% vs. 19.9 ± 6.06%; P < 0.05). These results suggest that uterine arteries from rats with T2D show reduced sensitivity of uterine vascular smooth muscle sGC to NO. During pregnancy, the GK uterine vascular smooth muscle fails to show relaxation responses similar to those of arteries from nondiabetic rats.
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Gombos, Randi B., and Denise G. Hemmings. "Differential effects on nitric oxide-mediated vasodilation in mesenteric and uterine arteries from cytomegalovirus-infected mice." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 4 (October 2010): H1124—H1134. http://dx.doi.org/10.1152/ajpheart.01113.2009.
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Chronic cytomegalovirus (CMV) infections are implicated in vascular diseases. Recently, we showed that an active mouse CMV (mCMV) infection in nonpregnant mice increased endothelial-dependent vasodilation in isolated mesenteric and uterine arteries. In late pregnancy, while increased vasodilation was found in mesenteric arteries from infected mice, there was a dramatic decrease in uterine arteries. Understanding the mechanisms for these vascular changes during CMV infections is important for pregnancy outcomes and long-term consequences of this chronic infection. Increased nitric oxide (NO) is implicated in CMV-associated atherosclerosis, and CMV replication is dependent on prostaglandin H synthase (PGHS) activity. Alternatively, CMV infections decrease NO under inflammatory conditions. We therefore hypothesized that changes in the contribution by NO or PGHS-induced vasodilators would explain the increased or decreased endothelial-dependent vasodilation in arteries from nonpregnant and late pregnant mice, respectively. We found that the contribution by NO to methacholine-induced vasodilation was significantly increased in mesenteric, but not uterine, arteries isolated from nonpregnant and pregnant mCMV-infected mice. Prostaglandin inhibition did not affect endothelial-dependent vasodilation in any group. Vasodilation responses to sodium nitroprusside, an NO donor, were increased in mesenteric and uterine arteries isolated only from mCMV-infected nonpregnant mice. These results explain the increased vasodilation responses observed in mesenteric arteries from mCMV-infected mice; however, the decreased vasodilation in uterine arteries from pregnant mice could not be explained by these mechanisms. Thus CMV infection affects the contribution of NO differently in endothelial-dependent vasodilation in pregnant compared with nonpregnant mice and also in the mesenteric compared with the uterine vascular bed.
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Burger, Natalie Z., Olga Y. Kuzina, George Osol, and Natalia I. Gokina. "Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca2+." American Journal of Physiology-Endocrinology and Metabolism 296, no. 3 (March 2009): E503—E512. http://dx.doi.org/10.1152/ajpendo.90517.2008.
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Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in the regulation of vascular microcirculatory tone. This study explores the role of estrogen in controlling EDHF-mediated vasodilation of uterine resistance arteries of the rat and also analyzes the contribution of endothelial cell (EC) Ca2+ signaling to this process. A parallel study was also performed with mesenteric arteries to provide comparison with a nonreproductive vasculature. Mature female rats underwent ovariectomy, with one half receiving 17β-estradiol replacement (OVX+E) and the other half serving as estrogen-deficient controls (OVX). Uterine or mesenteric resistance arteries were harvested, cannulated, and pressurized. Nitric oxide and prostacyclin production were inhibited with 200 μM NG-nitro-l-arginine and 10 μM indomethacin, respectively. ACh effectively dilated the arteries preconstricted with phenylephrine but failed to induce dilation of vessels preconstricted with high-K+ solution. ACh EC50 values were decreased by estrogen replacement by five- and twofold in uterine and mesenteric arteries, respectively. As evidenced by fura-2-based measurements of EC cytoplasmic Ca2+ concentration ([Ca2+]i), estrogen replacement was associated with increased basal and ACh-stimulated EC [Ca2+]i rise in uterine, but not mesenteric, vessels. These data demonstrate that EDHF contributes to endothelium-dependent vasodilation of uterine and mesenteric resistance arteries and that estrogen controls EDHF-related mechanism(s) more efficiently in reproductive vs. nonreproductive vessels. Enhanced endothelial Ca2+ signaling may be an important underlying mechanism in estrogenic modulation of EDHF-mediated vasodilation in small resistance uterine arteries.
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Gombos, R. B., V. Wolan, K. McDonald, and D. G. Hemmings. "Impaired vascular function in mice with an active cytomegalovirus infection." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (April 2009): H937—H945. http://dx.doi.org/10.1152/ajpheart.01027.2008.
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Human cytomegalovirus (CMV) is implicated in vascular complications through endothelial dysfunction. However, the effect of in vivo infections on vascular function in isolated arteries has not been examined. In pregnancy, systemic and uterine vascular adaptations accommodate increased blood volume through several mechanisms, including decreased sensitivity to vasoconstrictors and increased production of endothelial-dependent vasodilators. We hypothesized that an active in vivo CMV infection would reduce vasodilation of isolated arteries to the endothelial-dependent vasodilator methacholine and increase vasoconstriction to the α1-adrenergic receptor agonist phenylephrine and that these CMV-induced changes would be accentuated in late pregnancy. A mouse CMV infection model was used to study vascular responses in isolated mesenteric and uterine arteries from nonpregnant and late pregnant mice. In the mouse, CMV is not transmitted to the fetus. Accordingly, there was no evidence of active infection in any fetus examined, even though an active infection was found in salivary glands, uterine and mesenteric arteries, and placentas. Contrary to our hypothesis, increased endothelial-dependent vasodilation was found in mesenteric arteries from infected compared with uninfected nonpregnant and pregnant mice These data implicate active CMV infections in hypotensive disorders. Similarly, increased vasodilation was found in uterine arteries from infected vs. uninfected nonpregnant mice. However, this was completely reversed in infected compared with uninfected late pregnant mice in which vasodilation in uterine arteries was significantly reduced. Uterine arteries from infected pregnant mice also showed increased vasoconstriction to phenylephrine. Maternal infection led to decreased placental weights but had no effect on fetal weights in late pregnancy. These novel data demonstrate abnormal systemic and uterine vascular responses during an active CMV infection in both nonpregnant and late pregnant mice. Importantly, despite reduced placental weights, fetal weights were maintained, suggesting effective intrauterine compensation in the mouse model.
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Hilgers, Rob H. P., Suzanne Oparil, Wout Wouters, and Herjan J. T. Coelingh Bennink. "Vasorelaxing effects of estetrol in rat arteries." Journal of Endocrinology 215, no. 1 (July 13, 2012): 97–106. http://dx.doi.org/10.1530/joe-12-0009.
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This study comparedex vivorelaxing responses to the naturally occurring human hormone estetrol (E4) vs 17β-estradiol (E2) in eight different vascular beds. Arteries were mounted in a myograph, contracted with either phenylephrine or serotonin, and cumulative concentration-response curves (CRCs) to E4and E2(0.1–100 μmol/l) were constructed. In all arteries tested, E4had lower potency than E2, although the differential effect was less in larger than smaller arteries. In uterine arteries, the nonselective estrogen receptor (ER) blocker ICI 182 780 (1 μmol/l) caused a significant rightward shift in the CRC to both E4and E2, indicating that the relaxation responses were ER dependent. Pharmacological blockade of nitric oxide (NO) synthases byNω-nitro-l-arginine methyl ester (l-NAME) blunted E2-mediated but not E4-mediated relaxing responses, while inhibition of prostaglandins and endothelium-dependent hyperpolarization did not alter relaxation to either E4or E2in uterine arteries. Combined blockade of NO release and action withl-NAME and the soluble guanylate cyclase (sGC) inhibitor ODQ resulted in greater inhibition of the relaxation response to E4compared with E2in uterine arteries. Endothelium denudation inhibited responses to both E4and E2, while E4and E2concentration-dependently blocked smooth muscle cell Ca2+entry in K+-depolarized and Ca2+-depleted uterine arteries. In conclusion, E4relaxes precontracted rat arteries in an artery-specific fashion. In uterine arteries, E4-induced relaxations are partially mediated via an endothelium-dependent mechanism involving ERs, sGC, and inhibition of smooth muscle cell Ca2+entry, but not NO synthases or endothelium-dependent hyperpolarization.
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Goulopoulou, Styliani, Johanna L. Hannan, Takayuki Matsumoto, and R. Clinton Webb. "Pregnancy reduces RhoA/Rho kinase and protein kinase C signaling pathways downstream of thromboxane receptor activation in the rat uterine artery." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 12 (June 15, 2012): H2477—H2488. http://dx.doi.org/10.1152/ajpheart.00900.2011.
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During pregnancy, reduced vascular responses to constrictors contribute to decreased uterine and total vascular resistance. Thromboxane A2(TxA2) is a potent vasoconstrictor that exerts its actions via diverse signaling pathways, and its biosynthesis increases in preeclampsia. In this study, we hypothesized that maternal vascular responses to TxA2will be attenuated via Rho kinase, PKC, p38 MAPK, and ERK1/2 signaling pathways. Isolated ring segments of uterine and small mesenteric arteries from late pregnant (19–21 days) and virgin rats were suspended in a myograph, and isometric force was measured. Pregnancy did not affect uterine and mesenteric artery responses to the TxA2analog U-46619 (10−9–10−5M), but transduction signals associated with these contractions were different between pregnant and nonpregnant rats. Inhibition of Rho kinase (10−6M Y-27632) reduced sensitivity to U-46619 in virgin uterine vessels but did not inhibit these contractions in pregnant uterine arteries and had no effect on mesenteric vessels. Treatment of arterial segments with a PKC inhibitor (10−6M bisindolylmaleimide I) reduced U-46619-induced contractions in virgin uterine and mesenteric arteries and in pregnant mesenteric arteries. Pregnant uterine arteries, however, were unresponsive to PKC inhibition. Inhibition of ERK1/2 (10−5M PD-98059) and p38 MAPK (10−5M SB-203580) reduced U46619-induced contractions in nonpregnant vessels and in pregnant uterine and mesenteric vessels. These data suggest that normal pregnancy does not affect uterine and mesenteric contractile responses to TxA2but reduces the contribution of Rho kinase and PKC signaling pathways to these contractions in the uterine vasculature. In contrast, the role of ERK1/2 and p38 MAPK in U-46619-induced uterine contractions remains unchanged with pregnancy. TxA2-associated transduction signals and its regulators might present potential targets for the development of new treatments for preeclampsia and other pregnancy-associated vascular diseases.
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Sagili, Haritha, Nagarajan Krishnan, Anish Keepanasseril, Sathiya Priya, and Sunilkumar Devaraj. "Uterine artery embolization for uterine arterio-venous malformation." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 10, no. 7 (June 28, 2021): 2902. http://dx.doi.org/10.18203/2320-1770.ijrcog20212691.
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Uterine arteriovenous malformations (AVM) as a cause of abnormal uterine bleeding are listed under “not otherwise classified” in Palm-Coein classification, is an abnormal communication between an artery and vein without an intervening capillary bed resulting in increased pressure and high velocity in the venous system. We report the case of heavy menstrual bleeding in a thirty-five-year-old primiparous lady for five years with fourteen weeks sized uterus and six gm hemoglobin. Ultrasound revealed an enlarged uterus with tubular spaces and color doppler showed tubular anechoic structures, both within the myometrium, with low resistance and high-velocity pattern suggestive of uterine arteriovenous malformations. Because of nonresponse to medical management, uterine artery embolization was carried out following which she had significant reduction in menstrual bleeding emphasizing it as a differential diagnosis in all cases presenting with heavy menses. Uterine artery embolization appears to be an effective modality of treatment especially in women whose wish to preserve fertility.
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St-Louis, Jean, Benoît Sicotte, Annie Beauséjour, and Michèle Brochu. "Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake." Reproduction 131, no. 2 (February 2006): 331–39. http://dx.doi.org/10.1530/rep.1.00565.
Full textAbstract:
Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin–angiotensin–aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low- and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na+) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 μm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 μmol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.
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Rivera Mena, María José, Andrés Felipe Mercado González, María del Cisne Vega Cobos, and Gabriela Michelle Vanegas Contreras. "Doppler de arterias uterinas para tamizaje y prevención de preeclampsia." Tesla Revista Científica 3, no. 1 (January 16, 2023): e119. http://dx.doi.org/10.55204/trc.v3i1.e119.
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Introducción: La preeclampsia sigue siendo una de las patologías más frecuentes en el embarazo con una alta tasa de morbilidad y mortalidad tanto materna como fetal, sin embargo, las técnicas de ecografía Doppler han sido de gran ayuda en los últimos años y han permitido reconocer tempranamente cambios patológicos producidos en el feto frente a diferentes tipos de lesión, dejando que actúe de forma oportuna en la disminución de la de morbilidad y mortalidad neonatal.
Objetivos: Describir la utilidad de la ecografía Doppler de las arterias uterinas para el tamizaje y prevención de preeclampsia
Métodos: Se llevó a cabo una búsqueda sistemática de la bibliografía en las principales bibliotecas medicas electrónicas (PUBMED, Cochrane Library, Web of Science, Trip Database) en los últimos 15 años a partir de octubre del 2007 hasta Octubre del 2022 en humanos, utilizando términos DeCS y MeSH como: ultrasonography, doppler, uterine artery, diagnosis, screening y pre-eclampsia,
Resultados: Se incluyeron 28 revisiones bibliográficas, en donde constan: 11 ensayos clínicos, 5 revisiones, 5 estudios observacionales, 3 soportes de investigación, 2 metaanálisis, 1 estudio comparativo y 1 estudio de evaluación, que abarco todos los tipos de estudios.
Conclusión: La ecografía Doppler de las arterias uterinas combinado con marcadores maternos aumentan la tasa de detección de pre eclampsia, es una herramienta diagnóstica útil en las gestantes, mostrando así una mayor capacidad predictiva en el tamizaje de preeclampsia, disminuyendo de manera importante los procedimientos invasivos.
Palabras clave: Ultrasonografía Doppler, arteria uterina, diagnostico, pre eclampsia.
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Nelson, S. H., O. S. Steinsland, R. L. Johnson, M. S. Suresh, A. Gifford, and J. S. Ehardt. "Pregnancy-induced alterations of neurogenic constriction and dilation of human uterine artery." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 4 (April 1, 1995): H1694—H1701. http://dx.doi.org/10.1152/ajpheart.1995.268.4.h1694.
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The responses to electrical field stimulation (EFS) of perivascular nerves in human uterine arteries were characterized. The arteries were removed from pregnant and nonpregnant patients undergoing hysterectomy. Tetrodotoxin, guanethidine, and phentolamine blocked EFS (2 min, 80 V, 0.1-ms duration)-induced constriction. The constrictions and the endogenous norepinephrine levels were lower (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. When arterial rings were precontracted, the response to EFS was biphasic, consisting of an initial constriction followed by a postconstriction relaxation. The EFS-induced relaxation was endothelium independent and was greater (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. The relaxation was enhanced by guanethidine and superoxide dismutase, inhibited by nitric oxide synthase inhibitors, blocked by tetrodotoxin, and unaffected by atropine, propranolol, or indomethacin. The results demonstrate that human uterine arteries respond to EFS with contraction and relaxation and that these responses may be mediated, respectively, by norepinephrine and, in part, by nitric oxide released from periarterial nerves. The decrease in neuronally mediated uterine arterial constriction and the increase in dilation could be physiological mechanisms for ensuring appropriate uteroplacental perfusion.
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Han, Michelle N., Hugo Ramirez, Luis Ruvalcaba, Juan Luis Contreras, Atunga Nyachieo, and Edwin Ramirez. "Uterine Autotransplantation in the Nonhuman Primate With Preservation of the Uterine and Ovarian Vascular Pedicles." Reproductive Sciences 26, no. 10 (March 25, 2018): 1329–35. http://dx.doi.org/10.1177/1933719118765976.
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Purpose: To evaluate the technical feasibility of performing a uterine autotransplantation in the nonhuman primate while preserving the uterine and ovarian vascular pedicles. Methods: Eight (n = 8) female baboons at a primate research facility underwent a uterine autotransplant procedure with preservation of the vascular pedicles. The uterine arteries were separated from their amorphous tissue and skeletonized toward the internal iliac arteries bilaterally. A segment of the internal iliac artery was removed bilaterally along with both uterine arteries. Both ovarian veins were preserved to assist with the reperfusion of the uterine organ. Due to larger vascular pedicles in one of the primates, the uterine arteries were separated and reattached directly via end-to-end anastomosis. In another baboon, the deep uterine vein was used as a vascular pedicle rather than the ovarian vein on the left side due to adequate size and visualization. Results: Immediate tissue reperfusion occurred intraoperatively in 5 of the animals, with slower perfusion in 3 of the animals. Average warm ischemia time was 43.8 minutes while the average cold ischemia time was 174 minutes (2 hours, 54 minutes). Average total surgical time was 5.9 hours. All animals were sheltered into separate cages and monitored for behavior changes and food and drink consumption. Three of the primates expired immediately postoperatively, 2 from severe dehydration and 1 from gastric aspiration. Conclusions: This pilot study describes a modified surgical approach for uterine transplants in the nonhuman primate. This surgical technique may be applicable to living and deceased donor uterine transplantation.
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Hu, C. Y., and C. P. Robinson. "The Effects of Soman on Human Isolated Uterine Arteries." Human Toxicology 7, no. 2 (March 1988): 141–44. http://dx.doi.org/10.1177/096032718800700206.
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1 The effects of soman on the resting contractile tension of human uterine arteries, and on contractions of these arteries to vasoactive agents were investigated. 2 Soman did not alter the resting tension of helically-cut strips of human uterine arteries. 3 Soman did not alter concentration-response curves of the strips to noradrenaline, serotonin, potassium chloride or histamine. 4 Soman increased contractile tension of human uterine artery strips to subsequently added 1 μM noradrenaline. 5 It is possible that this enhancement may be involved in decreased regional blood flow following soman administration.
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Hu, X. Q., L. D. Longo, R. D. Gilbert, and L. Zhang. "Effects of long-term high-altitude hypoxemia on alpha 1-adrenergic receptors in the ovine uterine artery." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 3 (March 1, 1996): H1001—H1007. http://dx.doi.org/10.1152/ajpheart.1996.270.3.h1001.
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To elucidate the effects of chronic hypoxia on alpha 1-adrenergic receptor-mediated contractions of the uterine artery, we examined norepinephrine-induced contractions in tissues obtained from near-term (approximately 140 days gestation) pregnant ewes maintained near sea level (approximately 300 m) and at high altitude (3,820 m) from 30 days gestation. Compared with the sea-level controls, contractions induced by norepinephrine in main and fourth-branch uterine arteries of the high-altitude animals were significantly depressed. The norepinephrine dose-response curves were shifted to the right and the concentrations at which 50% of the maximal response was attained were increased 3.2- and 5.7-fold in the main and fourth-branch uterine arteries, respectively. The maximal responses were decreased 22 and 36% in main and fourth-branch uterine arteries, respectively. The dissociation constants of norepinephrine were increased from 0.77 to 1.53 microM and from 0.72 to 2.05 microM in main and fourth-branch uterine arteries, respectively. Radioligand binding studies with [3H]prazosin revealed a decrease in the density of alpha 1-adrenergic receptors in both vessels from high-altitude animals. We conclude that chronic hypoxia depresses alpha 1-adrenergic receptor-induced contractions of conduit- and resistance-type uterine arteries. The depressed contractility is mediated, at least in part, by decreases in alpha 1-adrenergic receptor density and agonist binding affinity.
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Springer, Stephanie, Mariella Polterauer, Maria Stammler-Safar, Harald Zeisler, Heinz Leipold, Christof Worda, and Katharina Worda. "Notching and Pulsatility Index of the Uterine Arteries and Preeclampsia in Twin Pregnancies." Journal of Clinical Medicine 9, no. 8 (August 15, 2020): 2653. http://dx.doi.org/10.3390/jcm9082653.
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Increased uterine artery Doppler indices have been shown to be associated with preeclampsia and adverse pregnancy outcomes in singleton and twin pregnancies. At 20–22 weeks of gestation, we assessed the use of notching, the highest, lowest, and mean pulsatility index (PI), and the combination of notching and PI of the uterine arteries to screen for preeclampsia. This was done in a cohort of 380 twin pregnancies. The results showed that the combination of notching and the highest PI above the 95th centile of the uterine arteries gives the best screening characteristics for preeclampsia in twin pregnancies. We calculated sensitivities for preeclampsia for notching, highest PI, and the combination of notching and the highest PI of 50%, 45% and 91%, with specificities of 96%, 96% and 93%, respectively. The present findings demonstrate that notching, increased highest PI, and the combination of notching and the highest PI of the uterine arteries is associated with an increased risk of preeclampsia in twin pregnancies. We observed the highest sensitivity and specificity by using the combination of notching and the highest PI of the uterine arteries.
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Gokina, Natalia I., and Tara Goecks. "Upregulation of endothelial cell Ca2+ signaling contributes to pregnancy-enhanced vasodilation of rat uteroplacental arteries." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 5 (May 2006): H2124—H2135. http://dx.doi.org/10.1152/ajpheart.00813.2005.
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Normal pregnancy is characterized by an increased uterine blood flow due to growth and remodeling of the maternal uterine vasculature and enhanced vasodilation of the uterine arteries. The objective of the present study was to examine the role of endothelial cell Ca2+ signaling in augmented endothelium-mediated vasodilation of uteroplacental arteries in late pregnancy. We performed fura-2-based measurements of the intracellular Ca2+ concentration ([Ca2+]i) in the cytoplasm of endothelial cells simultaneously with diameter in pressurized uterine arteries from nonpregnant (NP) and late-pregnant (LP) rats. Basal levels of endothelial cell [Ca2+]i were higher in arteries from LP rats compared with NP controls. Withdrawal of extracellular Ca2+ resulted in a decrease in the level of basal [Ca2+]i that was significantly larger in arteries of LP than NP rats. The rate of Mn2+-induced quenching of fura-2 fluorescence was significantly elevated in late pregnancy, implicating augmented Ca2+ influx as a cause of increased basal levels of [Ca2+]i in endothelial cells. Elevation of intraluminal pressure resulted in a transient increase in endothelial [Ca2+]i that was markedly potentiated in late gestation. ACh-induced [Ca2+]i and vasodilator responses were significantly augmented in arteries of LP compared with NP rats and were abolished by BAPTA treatment, demonstrating a critical role of [Ca2+]i elevation in the production of endothelium-derived vasodilators. Together, these results indicate that late pregnancy is a state of enhanced basal and stimulated Ca2+ signaling in endothelial cells of uterine vessels, which may represent an important underlying mechanism for augmented vasodilation in the maternal uterine circulation.
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El-Sherbiny, H., K. H. El-Shahat, A. M. Abo El-Maaty, and E. A. Abdelnaby. "Ovarian and uterine haemodynamics and their relation to steroid hormonal levels in postpartum Egyptian buffaloes." BULGARIAN JOURNAL OF VETERINARY MEDICINE 25, no. 2 (2022): 262–73. http://dx.doi.org/10.15547/bjvm.2020-0091.
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The current study aimed to assess the ovarian and uterine haemodynamics in postpartum (pp) Egyptian buffaloes and their relation to steroid hormonal levels (progesterone and estrogen). Six multiparous buffalos with normal calving were examined by using trans-rectal Doppler sonography to assess the blood flow in ipsilateral and contralateral ovarian and uterine arteries. Doppler parameters viz. peak systolic velocity (PSV), blood flow volume (BFV), resistance (RI) and pulsatility index (PI) were measured at 1st till 6th postpartum weeks. In addition, diameters (mm) of the ovarian and uterine arteries and the vascularisation area (mm2) of ovary were determined. The blood samples were collected starting from 1st week post calving and every week thereafter following each ultrasound Doppler examination for assay of progesterone and estradiol. Results indicated that PI and RI increased consistently and significantly (P<0.05) till the 6th week post calving as compared to those recorded at 1st week in ipsilateral ovarian and uterine arteries. However, the blood flow volume and peak systolic velocity in both ovarian and uterine arteries decreased gradually from 1st week till the 6th week after calving. There were very strong positive correlations between PSV and BFV, in both ipsilateral and contralateral ovarian and uterine arteries. Blood concentrations of progesterone were lower (P<0.05) during the first four weeks than those recorded at 5th and 6th postpartum weeks. This trend was reversed for blood estradiol 17-β. The results of the present investigation concluded that Doppler ultrasonography is a suitable tool for assessing changes in ovarian and uterine perfusion during the puerperium.
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Itoh, Hiroaki, Ian M. Bird, Kazuwa Nakao, and Ronald R. Magness. "Pregnancy Increases Soluble and Particulate Guanylate Cyclases and Decreases the Clearance Receptor of Natriuretic Peptides in Ovine Uterine, But Not Systemic, Arteries*." Endocrinology 139, no. 7 (July 1, 1998): 3329–41. http://dx.doi.org/10.1210/endo.139.7.6093.
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Abstract Pregnancy increases uterine blood flow by 30- to 50-fold and uterine production of cGMP by 38-fold. Moreover, cGMP causes potent vasodilatation. We hypothesized that pregnancy up-regulates soluble and particulate guanylate cyclases (sGC and pGC) in ovine uterine arteries. Activities of sGC and pGC were compared by measuring cGMP production (37 C; 10 min) by uterine arteries from nonpregnant (n = 5) and pregnant (n = 4, 120 ± 2 days’ gestation; term = 145 ± 3 days; mean ± se) ewes after sodium nitroprusside (100 μm), atrial natriuretic peptide (1μ m), or C-type natriuretic peptide (CNP; 1μ m) treatment. The protein and/or messenger RNA expressions of sGC β1-subunit, pGC-A, pGC-B, the clearance receptor of natriuretic peptide (CR), and CNP were investigated in uterine and systemic (renal and/or omental) arteries from nonpregnant (n = 29) and pregnant (n = 21; 125 ± 2 days’ gestation) ewes. The potencies of uterine arterial GC activities were sGC ≫ pGC-A> pGC-B. Activities as well as protein expression of sGC, pGC-A, and pGC-B in pregnant uterine arteries were increased 48–128% above those in nonpregnant controls concomitant with a 34% down-regulation of CR protein expression; systemic arterial protein expressions were unaltered. These changes in uterine arterial GC-B and CR were confirmed using RT-PCR. Immunohistochemical staining of CNP in uterine, but not systemic, arterial endothelium from pregnant ewes was much stronger than that from nonpregnant ewes. Thus, two distinct GC pathways are present in ovine uterine artery, and both may be specifically up-regulated during pregnancy and so contribute to the tremendous local increase in cGMP production during pregnancy.
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Kozlov, S. V., D. D. Dvoretskii, L. A. Alekseenko, A. Omelchenko, and V. D. Kartamysheva. "Anatomical Variants of Uterine Arteries." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 3, no. 4 (May 18, 2018): 32–37. http://dx.doi.org/10.26693/jmbs03.04.032.
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Schilke, Candice J., and Kim Michael. "Pseudoaneurysm of the Uterine Arteries." Journal of Diagnostic Medical Sonography 21, no. 3 (May 2005): 257–61. http://dx.doi.org/10.1177/8756479305275484.
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Scott, Kayley, Hannah L. Morgan, Christian Delles, Simon Fisher, Delyth Graham, and Martin W. McBride. "Distinct uterine artery gene expression profiles during early gestation in the stroke-prone spontaneously hypertensive rat." Physiological Genomics 53, no. 4 (April 1, 2021): 160–71. http://dx.doi.org/10.1152/physiolgenomics.00159.2020.
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During pregnancy, the uterine spiral arteries undergo major vascular remodeling to ensure sufficient uteroplacental perfusion to support the fetus. In pregnancies complicated by hypertensive disorders, this remodeling is deficient leading to impaired uteroplacental blood flow and poor maternal and fetal outcomes. The underlying genetic mechanisms for failed vascular remodeling are not fully understood. This study aimed to examine the early-pregnancy-associated gene changes in the uterine arteries of spontaneously hypertensive stroke-prone rats (SHRSP) compared with their normotensive counterparts, Wistar–Kyoto rats (WKY). Uterine arteries from gestational day 6.5 WKY and SHRSP were processed for RNA-sequencing, along with virgin, age-matched controls for each strain. Gene expression changes were identified and biological pathways were implicated and interpretated using ingenuity pathway analysis (IPA). This study found that WKY uterine arteries from early pregnancy exhibit a gene expression pattern that is suggestive of a pregnancy-dependent reduction in Ca2+ handling and renin-angiotensin-aldosterone system (RAAS) components and an increase in ATP production. In contrast, the expression pattern of pregnant SHRSP uterine arteries was dominated by an elevated immune response and increased production of reactive oxygen species (ROS) and downstream effectors of the RAAS. These results suggest that in a rat model, hypertension during pregnancy impacts uterine artery gene expression patterns as early as the first week of pregnancy. The pathway changes involved may underlie or contribute to the adverse vascular remodeling and resultant placental ischemia and systemic vascular dysfunction observed in SHRSP in late gestation.
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Amini, Marjan, Mahnaz Ranjkesh, Saba Nikanfar, Amir Fattahi, Laya Farzadi, and Kobra Hamdi. "Alterations of Uterine Blood Flow During the Follicular Phase in Patients With Recurrent Implantation Failure: A Doppler Ultrasonographic Study." International Journal of Women's Health and Reproduction Sciences 9, no. 3 (June 4, 2021): 217–21. http://dx.doi.org/10.15296/ijwhr.2021.40.
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Objectives: The dynamics of blood flow in the endometrium plays a crucial role during the implantation process. This study aimed to assess the uterine perfusion during the follicular phase in patients with a history of recurrent implantation failure (RIF) and healthy fertile women using the transvaginal ultrasound color Doppler method. Materials and Methods: To this end, 50 patients with RIF and 50 age-matched healthy fertile women were recruited in this case-control study. The transvaginal color Doppler ultrasonography was used to evaluate the pulsatility index (PI) and resistance index (RI) of the uterine, arcuate, and sub-endometrial arteries during the follicular phase in both groups. Results: The RI and PI of both right and left uterine arteries were higher in the RIF group compared to the fertile women (P<0.05). Our results showed that the PI and RI of sub-endometrial blood flow and the RI of arcuate arteries were substantially higher in the group with a history of RIF in comparison with the control group. However, the PI of arcuate arteries was not significantly different between the groups. Conclusions: Adequate uterine perfusion and sub-endometrial blood flow are necessary to achieve successful implantation and pregnancy since our results demonstrated the higher resistance of uterine and sub-endometrial arteries in patients with a history of RIF. Thus, the assessments of uterine perfusion indices during the follicular phase could be used as a non-invasive method in the evaluation of patients with RIF.
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Meziani, Ferhat, Angela Tesse, Sandra Welsch, Hélène Kremer, Mariette Barthelmebs, Ramaroson Andriantsitohaina, Francis Schneider, and Alexis Gairard. "Expression and Biological Activity of Parathyroid Hormone-Related Peptide in Pregnant Rat Uterine Artery: Any Role for 8-Iso-Prostaglandin F2α?" Endocrinology 149, no. 2 (November 29, 2007): 626–33. http://dx.doi.org/10.1210/en.2007-0568.
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PTHrP is produced in vessels and acts as a local modulator of tone. We recently reported that PTHrP(1–34) is able to induce vasorelaxation in rat uterine arteries, but in pregnancy, this response is blunted and becomes strictly endothelium dependent. The present study aimed to get insights into the mechanisms involved in these changes because the adaptation of uterine blood flow is essential for fetal development. On d 20 of gestation, RT-PCR analysis of uterine arteries showed that PTH/PTHrP receptor (PTH1R) mRNA expression was decreased, whereas that of PTHrP mRNA was increased. This was associated with a redistribution of the PTHrP/PTH1R system, with both PTH1R protein and PTHrP peptide becoming concentrated in the intimal layer of arteries from pregnant rats. On the other hand, the blunted vasorelaxation induced by PTHrP(1–34) in uterine arteries from pregnant rats was specifically restored by indomethacin and a specific cyclooxygenase-2 inhibitor, NS 398. This was associated with an increase in cyclooxygenase-2 expression and in 8-iso-prostaglandin F2α release when uterine arteries from pregnant rats were exposed to high levels of PTHrP(1–34). Most interestingly, 8-iso-prostaglandin F2α itself was able to increase PTHrP expression and reduce PTH1R expression in cultured rat aortic smooth muscle cells. These results suggest a local regulation of uterine artery functions by PTHrP during pregnancy resulting from PTH1R redistribution. Moreover, they shed light on a potential role of 8-iso-prostaglandin F2α.