"Sulprostone"

Study of Predictors of Failure of Sulprostone Treatment in Postpartum Hemorrhage The investigators wish to identify potential factors predicting failure of second-line drug treatment (sulproston (Nalador®)): risk factors and factors linked to a failure to take initial care for PPH.A better understanding of the aggravating factors of HPP and more particularly the factors inherent to the initial

administration and higher gravidity and parity [95,96]. Alternate regimens Alternative prostaglandin analogs. Early management regimens for EPL included various prostaglandin analogs, including PGE1 analogs (gemeprost and misoprostol), PGE2 analogs (sulprostone and dino-prostone), and the PGF2α analog carboprost [97–105]. The use of misoprostol eventually became favored among prostaglandin ana-logs for its low

vaginally at 35-42 weeks of gestation. Inclusion criteria were a postpartum hemorrhage refractory to first-line uterotonic (oxytocin) and requiring a second-line uterotonic treatment with sulprostone (E1 prostaglandin). In the study group, the sulprostone infusion was combined with intrauterine tamponade by an ebb® balloon performed within 15 minutes of randomization. In the control group, the sulprostone infusion was started alone within 15 minutes of randomization, and if bleeding persisted 30 minutes after the sulprostone infusion started, intrauterine tamponade by the ebb® balloon was performed. In both groups, if the bleeding persisted 30 minutes after the insertion of the balloon, an emergency radiological or surgical invasive procedure was performed. The primary outcome was the proportion of women

Cardiac arrest during sulprostone administration - a case report. Sulprostone, a synthetic prostaglandin analogue with potent uterotonic action, has been shown to have a low complication rate in a large series. We present a case of cardiac arrest in a parturient after Caesarean section during continuous infusion of intravenous sulprostone administered for atonic post-partum haemorrhage. She had cardiopulmonary resuscitation for 25 min before spontaneous circulation returned. The sequence of events, the results of investigations carried out during the intensive care unit stay, and the presence of multiple cardiovascular risk factors, suggest that sulprostone caused coronary spasm, bradycardia, and subsequent asystole, similar to other cases described in the literature.

modulation of Itga4-VCAM1 binding. EP3 upregulated Itga4 expression in NK cells through promoting Spic nuclear translocation via PKC-mediated phosphorylation of Spic at T191. Activation of EP3 by sulprostone alleviated CCL4-induced liver fibrosis in mice. Thus, EP3 is required for adhesion and cytotoxicity of NK cells toward HSCs and may serve as a therapeutic target for the management of LF.

Stimulation of the EP₃ receptor causes lung oedema by activation of TRPC6 in pulmonary endothelial cells. Prostaglandin E (PGE) increases pulmonary vascular permeability by activation of the PGE receptor 3 (EP), which may explain adverse pulmonary effects of the EP/EP receptor agonist sulprostone in patients. In addition, PGE contributes to pulmonary oedema in response to platelet -mediated TRPC6 recruitment in PAF-induced lung oedema. In isolated lungs, we measured increases in endothelial calcium (ΔCa) or lung weight (Δweight), and endothelial caveolar TRPC6 abundance as well as phosphorylation. PAF-induced ΔCa and Δweight were attenuated in EP-deficient mice. Sulprostone replicated PAF-induced ΔCa and Δweight which were blocked by pharmacological/genetic inhibition of TRPC6

effect is uncertain.Sulprostone is a potent stimulator of uterine smooth muscle contractions with high abortifacient activity. It is not licensed in the UK but has been shown in one small study (n=50) to reduce the need for the manual removal of the placenta by 49%[9]and in a study of 126 women, all of whom received sulprostone, by 39.7%.Misoprostol does not reduce the need for manual removal . doi: 10.1002/14651858.CD004904.pub3.Nardin JM, Weeks A, Carroli G; Umbilical vein injection for management of retained placenta. Cochrane Database Syst Rev. 2011 May 11(5):CD001337. doi: 10.1002/14651858.CD001337.pub2.van Beekhuizen HJ, de Groot AN, De Boo T, et al; Sulprostone reduces the need for the manual removal of the placenta in patients with retained placenta: a randomized controlled trial

after chronic infection. Prostaglandins E2 (PGE2) production was significantly elevated in INS-1E after long-term E. coli infection and the restored insulin secretion in presence of L798106, a specific EP3 antagonist, and NS-398, a COX-2 inhibitor, and the reduction of insulin secretion in presence of sulprostone, a specific EP3 agonist, revealed their involvement in the effects triggered by bacterial

to the control group in first-trimester placentas. we demonstrated that sulprostone (an EP1/EP3 agonist) inhibited the secretion of beta-hCG and progesterone in JEG-3 cells and the secretion of beta-hCG in HTR-8/SVneo cells while it induced the expression of plasminogen activator inhibitor type 1 in JEG-3 cells. In addition, PGE/sulprostone was able to stimulate the expression of G, phosphorylated

, and the administration of 5-10 IU oxytocin injected slowly IV or IM, followed by a maintenance infusion not to exceed a cumulative dose of 40IU (professional consensus). If oxytocin fails to control the bleeding, the administration of sulprostone is recommended within 30minutes of the PPH diagnosis (Grade C). Intrauterine balloon tamponade can be performed if sulprostone fails and before recourse to either surgery plasma (FFP) may be administered without awaiting laboratory results (professional consensus). Tranexamic acid may be used at a dose of 1 g, renewable once if ineffective the first time in the treatment of PPH when bleeding persists after sulprostone administration (professional consensus), even though its clinical value has not yet been demonstrated in obstetric settings. It is recommended to prevent

Impact of uterine balloon tamponade on the use of invasive procedures in severe postpartum hemorrhage. The aim of this study was to assess the impact of tamponade when uterotonic agents fail, on the need for surgery or interventional radiology. All women who received sulprostone for postpartum hemorrhage were retrospectively compared over two periods [December 2008 to December 2010 without use of tamponade (period 1) and June 2011 to June 2013 with use of tamponade (period 2)] in the case of sulprostone failure (STROBE compliant retrospective cohort study). During period 2, interventional radiology or surgery was used only in the case of tamponade failure. 165 women were included (74 for period 1, 91 for period 2). The rate of interventional radiology or surgery significantly decreased from period

trinor Prostaglandin E2 ethyl amide), EP2 (Butaprost), EP3 (Sulprostone) and EP4 (CAY10598) and antagonists of EP1 (SC-19220), EP2 (AH6809) and EP4 (L-161982) at different concentrations, respectively. The neuronal viability, lactate dehydrogenase leakage rate and PGE2 content were detected by MTT assay, lactate dehydrogenase assay kit and enzyme-linked immunosorbent assay, respectively. The mRNA

signaling mechanisms. β-cell proliferation was assessed in mouse and human islets treated with selective agonists and antagonists for EP3 (sulprostone and DG-041, respectively) and EP4 (CAY10598 and L-161,982, respectively). β-cell survival was measured in mouse and human islets treated with the EP3- and EP4-selective ligands in conjunction with a cytokine cocktail to induce cell death. Changes in gene

concentrate compared to the current practice based on late administration in severe PPH patients requiring second line uterotonics. This is a prospective multicentre, randomised, double-blind, placebo-controlled trial. A total of 412 patients will be randomised if they meet the following criteria: female patients≥18 years old, vaginal delivery, PPH requiring IV administration of prostaglandins (sulprostone

indicated that Ep 3 (-/-) and WT-STZ CDs responded to AVP stimulation similarly to those of wild-type mice, with a 60% increase in fluid reabsorption. In WT non-injected and WT-STZ mice, EP3 activation with sulprostone (PGE2 analogue) abrogated AVP-mediated water reabsorption; this effect was absent in mice lacking EP3. A major finding of this work is that Ep 3 (-/-)-STZ mice showed blunted renal

pulp cells were exposed to PGE2 and 19R-OH PGE2 (EP2 agonist) or sulprostone (EP1/EP3 agonist) for 5 to 40 minutes. Cellular cyclic adenosine monophosphate (cAMP) levels were measured using the enzyme-linked immunosorbent assay. In some experiments, cells were pretreated with SQ22536 (adenylate cyclase inhibitor), H89 (protein kinase A inhibitor), dorsomorphin (adenosine monophosphate-activated protein kinase inhibitor), U73122 (phospholipase C inhibitor), thapsigargin (inhibitor of intracellular calcium release), W7 (calmodulin antagonist), verapamil (L-type calcium channel blocker), and EGTA (extracellular calcium chelator) for 20 minutes before the addition of PGE2. PGE2 and 19R-OH PGE2 (EP2 agonist) stimulated cAMP production, whereas sulprostone (EP1/EP3 agonist) shows little effect. PGE2