Korean J Urol.
2005 Sep;46(9):981-991.
Blood Flow and Genetic Expression Changes of the Rat Bladder to Short Term Partial Outlet Obstruction
- Affiliations
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- 1Department of Urology, Park Young Soo Urologic Clinic, Korea.
- 2Department of Urology, College of Medicine, Pusan National University, Busan, Korea. toohotman@hanmail.net
Abstract
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PURPOSE: This study was aimed at evaluating the expressions of types I and III collagen, inducible nitric oxide synthase (iNOS), hypoxic inducible factor-1alpha(HIF-1alpha), vascular endothelial growth factor (VEGF) and the hemodynamic changes of the bladder during the acute stages of a partial bladder outlet obstruction (PBOO) in adult rats.
MATERIALS AND METHODS
Bladder specimens were aseptically removed from 35 Sprague-Dawley adult rats (8 week old, weight 250-300gm) of both sham and experimental groups at 6, 12 and 24 hours, and 2, 3, 5 and 7 days after establishing a partial bladder outlet obstruction. Bladder blood flow was measured at the left vesicular artery using a laser flowmeter. The expressions of types I and III collagen, iNOS, HIF-1alpha and VEGF in relation to changes of the bladder wall were evaluated by immunohistochemical staining and Western blot assay.
RESULTS
There was a significant difference in the vesical blood flow between the sham and experimental groups after the establishment of a PBOO. The bladder blood flow of the experimental groups was significantly decreased after establishing a PBOO of 3 days duration. The expressions of type III collagen and iNOS from the immunohistochemical staining of the bladder were markedly increased during the acute stages of a PBOO. The expressions of HIF-1alpha and VEGF from the Western blot of the bladder increased with duration of the obstruction.
CONCLUSIONS
A decreased bladder blood flow during the acute stages of PBOO generally enhanced the expressions of iNOS and type III collagen. This study suggests that hypoxia of the bladder after establishing a PBOO induces the expression of HIF-1alpha, and then enhances the production of nitric oxide (NO) due to activation of iNOS, which finally results in bladder growth and a decrease in bladder wall compliance.