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J Urol. 2001 May;165(5):1745-7.

Bladder dysfunction after acute urinary retention in rats.

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  • 1Department of Urology, Tottori University Faculty of Medicine, Yonago, Tottori, Japan.



We investigated bladder function in acute urinary retention and subsequent catheterization in rat bladders.


The penile urethra in rats was clamped with a small clip and cystostomy was performed to infuse 3 ml. of saline for inducing acute urinary retention. At 30 minutes after the induction of urinary retention the cystostomy was opened to empty the bladder. In functional studies contractile responses to carbachol were measured in group 1-before, group 2-at 3 ml. of urinary retention, group 3-at 3 ml. of urinary retention exposed for 30 minutes and group 4-30 minutes after catheterization. Moreover, in vivo real-time monitoring of blood flow and vesical pressure were measured in the bladders with a laser Doppler flowmeter and cystometrography, respectively. Malonaldehyde and 4-hydroxyalkenals were measured by colorimetric assay in these groups.


In functional studies the mean maximum contractile response value plus or minus standard deviation of carbachol-to-bladder in groups 1 to 4 was 11.8 +/- 1.3, 11.9 +/- 1.7, 9.8 +/- 0.8 and 6.9 +/- 0.7 gm./mm.2, respectively. In real-time monitoring of blood flow and vesical pressure acute urinary retention significantly decreased blood flow and increased vesical pressure, and subsequent catheterization increased blood flow and decreased vesical pressure in the bladders. The concentrations of malonaldehyde and 4-hydroxyalkenals in the bladders in group 4 were significantly higher than in the other groups.


Our data indicate that bladder dysfunction after catheterization is partially caused by free radicals, which have an important role in bladder dysfunction during acute urinary retention.

[PubMed - indexed for MEDLINE]
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