Effects of long-term partial outflow obstruction on bladder function in the rat

✍ Scribed by Masahiko Saito; Masaharu Ohmura; Atsuo Kondo

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 489 KB
• Volume: 15
• Category: Article
• ISSN: 0733-2467
• DOI: 10.1002/(sici)1520-6777(1996)15:2<157::aid-nau5>3.0.co;2-e

✦ Synopsis

The effects of chronic partial outflow obstruction in rats were investigated. The urethra of male rats was partially obstructed for 3 or 6 months and bladder function was compared with that of age-matched controls. Bladder function was studied in vivo by infusion cystometry and in vitro by measuring the response of bladder muscle strips to stimulation. Cystometrograms of outflow-obstructed bladders were categorized into three types: type 1 was equivalent to a normal bladder; type 2 was characterized by large capacity, enhanced voiding pressure, and some residual urine; type 3 had the largest capacity, an impaired voiding pressure, and considerable residual volume (overflow-type of incontinence). The type 3 bladder was the most frequently observed type in rats obstructed for 6 months. Bladder weight increased significantly in rats with outflow obstruction. When five in vivo cystometric parameters (pressure at which micturition was induced, capacity, maximum voiding pressure, voided urine volume, and residual urine volume) were analyzed according to duration of obstruction, only two parameters (capacity and residual urine volume) in rats obstructed for 6 months differed significantly from those in age-matched controls. Evaluation of these values according to cystometric type showed a significant deterioration in four of five parameters in type 3 bladders. Contractile responses of the bladder in vitro to field stimulation, bethanechol, ATP, and KCI were significantly impaired in those obstructed for 3 or 6 months. When in vitro responses were analyzed according to the classification of cystometric type, deterioration of contractility was confirmed in both types 2 and 3 bladders. The present animal model of outflow obstruction can serve as a model of benign prostatic hyperplasia in humans.