Studies in animals demonstrate the basis for an excitatory urethra to bladder reflex. Urethral stimulation by prostaglandin E2 induces an excitatory effect on micturition reflex by activation of C-fiber afferent nerves. α1A-adrenoceptor blocker has an inhibitory effect on the micturition FK866 reflex, suggesting excitatory urethra to bladder reflex is mediated by α1A-adrenoceptor. Even if there is no obstruction, increase in urethral sensory due to BPE may induce the development of the detrusor overactivity. “
“Objectives: We investigated the time
course of the stromal cell-derived factor 1α (SDF1α) expression and behavior of intravenously administered bone marrow-derived stromal (BMS) cells in the urinary bladder of partial bladder outlet obstruction (PBOO) rats. Methods: Study 1: Recombinant SDF1α or saline was directly injected into the bladder wall of female rats followed by intravenous administration of BMS cells isolated from green fluorescent protein (GFP) transgenic
rats. The bladder was examined with immunohistochemistry to determine whether SDF1α would enhance migration of BMS cells to the bladder. Study 2: Following surgery of PBOO or sham in female rats, bladders were removed on days 1–14, and expression of hypoxia inducible factor 1α (HIF1α) and SDF1α were examined with real-time polymerase chain reaction (PCR) to determine if PBOO preferentially increased their expression. Study 3: Female rats underwent PBOO or sham surgery followed by intravenous administration EPZ-6438 mw of GFP-positive BMS cells. Bladders were examined with immunohistochemistry on days 1–14 to determine whether mafosfamide BMS cells preferentially accumulated in the bladder. Results: BMS cells were accumulated in the injection site of SDF1α but not saline in the bladder. SDF1α and HIF1α increased at day 1 after PBOO compared to sham. More BMS cells accumulated in the bladder of PBOO on day 1, and some BMS cells expressed smooth muscle phenotypes by day 14. Conclusion: SDF1α induced with ischemia/hypoxia due to PBOO is implicated in the accumulation
of BMS cells in the bladder and regeneration of the bladder for PBOO. “
“Objectives: Ketamine abuse can damage the urinary tract and cause lower urinary tract symptoms (LUTS). This report presents our observations and management on urinary tract damage caused by ketamine abuse. Methods: From November 2006 to February 2009, 20 patients visited Taipei Veterans General Hospital due to ketamine-related lower urinary tract symptoms. We analyzed the clinical presentations, daily ketamine dose, interval between ketamine usage to develop LUTS, urodynamic studies, radiological image findings, cystoscopic and ureterorenoscopic findings, histological findings, urinary ketamine levels and treatment responses.