Re: Griffiths C, Drinnan M, Harding C, et al. 2005. Comparison of invasive and non-invasive bladder pressure measurements by calculation of the bladder outlet obstruction index. Neurourol Urodynam 24:529–531

2007 ◽  
Vol 26 (3) ◽  
pp. 454-454
Author(s):  
Shyh-Jen Wang ◽  
Alex Tong-Long Lin ◽  
Chao-An Lin
Keyword(s):  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Bladder Pressure ◽  
Pressure Measurements ◽  
Non Invasive

scholarly journals Preventative effects of a HIF inhibitor, 17-DMAG, on partial bladder outlet obstruction-induced bladder dysfunction

2017 ◽  
Vol 313 (5) ◽  
pp. F1149-F1160 ◽  
Author(s):  
Nao Iguchi ◽  
M. İrfan Dönmez ◽  
Anna P. Malykhina ◽  
Alonso Carrasco ◽  
Duncan T. Wilcox
Keyword(s):  
Bladder Outlet Obstruction ◽  
Target Genes ◽  
Bladder Dysfunction ◽  
Pediatric Population ◽  
Outlet Obstruction ◽  
Bladder Function ◽  
Bladder Pressure ◽  
Partial Bladder Outlet Obstruction

Posterior urethral valves are the most common cause of partial bladder outlet obstruction (PBOO) in the pediatric population. Pathological changes in the bladder developed during PBOO are responsible for long-lasting voiding dysfunction in this population despite early surgical interventions. Increasing evidence showed PBOO induces an upregulation of hypoxia-inducible factors (HIFs) and their transcriptional target genes, and they play a role in pathophysiological changes in the obstructed bladders. We hypothesized that blocking HIF pathways can prevent PBOO-induced bladder dysfunction. PBOO was surgically created by ligation of the bladder neck in male C57BL/6J mice for 2 wk. PBOO mice received intraperitoneal injection of either saline or 17-DMAG (alvespimycin, 3 mg/kg) every 48 h starting from day 1 postsurgery. Sham-operated animals received injection of saline on the same schedule as PBOO mice and served as controls. The bladders were harvested after 2 wk, and basal activity and evoked contractility of the detrusor smooth muscle (DSM) were evaluated in vitro. Bladder function was assessed in vivo by void spot assay and cystometry in conscious, unrestrained mice. Results indicated the 17-DMAG treatment preserved DSM contractility and partially prevented the development of detrusor over activity in obstructed bladders. In addition, PBOO caused a significant increase in the frequency of micturition, which was significantly reduced by 17-DMAG treatment. The 17-DMAG treatment improved urodynamic parameters, including increases in the bladder pressure at micturition and nonvoid contractions observed in PBOO mice. These results demonstrate that treatment with 17-DMAG, a HIF inhibitor, significantly alleviated PBOO-induced bladder pathology in vivo.

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