Study Objectives: The primary objective is to determine the rate of morbid events (urinary tract infection, hematuria, urinary retention, false positive, incidental finding) associated with routine cystoscopies performed intraoperatively during total laparoscopic hysterectomies (TLH). The secondary objectives are 1) to determine the rate of urinary complications during TLHs in our centers and 2) to determine the detection rate of urinary complications using cystoscopy during TLHs.
Method: Descriptive retrospective multicenter study.
Objective: To review short- and long-term complications associated with intraoperative rupture of benign ovarian cysts.
Data Sources: The Cochrane Central Register of Controlled Trials, BIOSIS, Medline (Ovid), Web of Science, ClinicalTrials.gov, and Google Scholar were searched using the following terms and their combinations: "spillage," "rupture," "leakage," "ovarian cyst," "teratoma," "dermoid," "operative," "surgery," "outcome.
Br J Pharmacol
September 2013
Background And Purpose: The contribution of endothelin-1 (ET-1) in a B2KO mouse model of a high salt-induced arterial hypertension was investigated.
Experimental Approach: Wild-type (WT) or B2KO mice receiving a normal diet (ND) or a high-salt diet (HSD) were monitored by radiotelemetry up to a maximum of 18 weeks. At the 12th week of diet, subgroups under ND or HSD received by gavage the ETA antagonist A127722 during 5 days.
J Pharmacol Exp Ther
February 2009
The aim of this study was to identify the role of chymase in the conversion of exogenously administered Big endothelin-1 in the mouse in vivo. Real-time polymerase chain reaction analysis detected mRNA of mucosal mast cell chymases 4 and 5, endothelin-converting enzyme 1a, and neutral endopeptidase 24.11 in pulmonary, cardiac, and aorta homogenates derived from C57BL/6J mice, with the latter tissue expressing the highest levels of both chymase isoforms.
View Article and Find Full Text PDFCan J Physiol Pharmacol
August 2008
We hypothesized that constitutive endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) have opposite effects on the regulation of endothelin and its receptors. We therefore sought to determine whether deletions of iNOS or eNOS genes in mice modulate pressor responses to endothelin and the expression of ETA and ETB receptors in a similar fashion. Despite unchanged baseline hemodynamic parameters, anesthetized iNOS-/- mice displayed reduced pressor responses to endothelin-1, but not to that of IRL-1620, a selective ETB agonist.
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