AIMS: Partial bladder outlet obstruction (PBOO) results in marked contractile, biochemical, and histological alterations in the bladder. Our aim was to determine the time course of progressive PBOO in the rabbit and to find parameters that marked the shift to decompensation. MATERIALS AND METHODS: Twenty-four rabbits were subjected to 1, 2, 4, and 8 weeks of PBOO. Sham operated rabbits served as controls. At each time period, cystometry was performed and individual bladder strips were used for contractility studies. Full-thickness sections of bladder body from each rabbit were fixed in formalin and used to determine the vascular density and nerve density. The balance of the bladder body was separated between muscle and mucosa and was analyzed for superoxide dismutase (SOD) and catalase (CAT) activities. RESULTS: Bladder weight increased progressively and all contractile responses were reduced significantly over the course of obstruction. Markedly increased bladder weight and very large bladder volumes indicated decompensation. Nerve density was marked decreased in decompensated bladders. Similarly, SOD activity in muscle decreased progressively and was markedly lower in decompensated bladders. Although CAT activity of the muscle increased after 2-4 weeks of obstruction, it decreased markedly in decompensated bladders. CONCLUSION: This study shows that prolonged PBOO causes progressive deterioration in the rabbit bladder with decompensation after 8 weeks. Markedly decreased nerve density and severely reduced SOD and CAT activities are associated with the shift from compensated to decompensated function of the bladder. They may be excellent biomarkers of decompensation. (c) 2007 Wiley-Liss, Inc.
AIMS: Partial bladder outlet obstruction (PBOO) results in marked contractile, biochemical, and histological alterations in the bladder. Our aim was to determine the time course of progressive PBOO in the rabbit and to find parameters that marked the shift to decompensation. MATERIALS AND METHODS: Twenty-four rabbits were subjected to 1, 2, 4, and 8 weeks of PBOO. Sham operated rabbits served as controls. At each time period, cystometry was performed and individual bladder strips were used for contractility studies. Full-thickness sections of bladder body from each rabbit were fixed in formalin and used to determine the vascular density and nerve density. The balance of the bladder body was separated between muscle and mucosa and was analyzed for superoxide dismutase (SOD) and catalase (CAT) activities. RESULTS:Bladder weight increased progressively and all contractile responses were reduced significantly over the course of obstruction. Markedly increased bladder weight and very large bladder volumes indicated decompensation. Nerve density was marked decreased in decompensated bladders. Similarly, SOD activity in muscle decreased progressively and was markedly lower in decompensated bladders. Although CAT activity of the muscle increased after 2-4 weeks of obstruction, it decreased markedly in decompensated bladders. CONCLUSION: This study shows that prolonged PBOO causes progressive deterioration in the rabbit bladder with decompensation after 8 weeks. Markedly decreased nerve density and severely reduced SOD and CAT activities are associated with the shift from compensated to decompensated function of the bladder. They may be excellent biomarkers of decompensation. (c) 2007 Wiley-Liss, Inc.