OBJECTIVES: To correlate the effect of bilateral in‐vivo bladder ischaemia/reperfusion on superoxide dismutase activity (SOD) and then to correlate this with contractile responses to various forms of stimulation. MATERIALS AND METHODS: Twenty mature male New Zealand White rabbits were divided into five equal groups: group 1 (controls); group 2, 2 h of in‐vivo bilateral bladder ischaemia; and groups 3–5, 2 h of in‐vivo ischaemia followed by 1, 7 or 14 days of reperfusion (recovery). At the end of the treatment period, bladder strips were incubated and placed in isolated baths for contractile studies. The contractile responses to field stimulation, carbachol (10 µmol/L), ATP and KCl were determined. The balance of the bladder body was separated into muscle and mucosa sections and analysed for SOD activity. RESULTS: There were few effects on contraction either directly after ischaemia or after 1 day of reperfusion. However, all contractile responses were significantly reduced at 7 and 14 days after ischaemia. SOD activity of the detrusor muscle was reduced significantly immediately after ischaemia and at 7 and 14 days of reperfusion. SOD activity of the mucosa was significantly greater than that of the muscle, and was significantly reduced by both ischaemia and all times of reperfusion. CONCLUSIONS: These studies show clearly that both ischaemia and reperfusion result in significantly lower activity of SOD, and in contractile dysfunctions, and that reperfusion results in greater decreases in both SOD activity and contractile responses than ischaemia alone.

Benign prostatic hyperplasia (BPH) is a disease that has its etiology in the abnormal growth of the adult human prostate gland that accompanies the aging process in men. The symptomatic presentation of this disease, however, is related largely to degenerative changes in the bladder that occur as a result of the increasing urethral resistance and partial bladder outlet obstruction (PBOO) caused by the growing prostate gland. BPH is characterized by bladder hypertrophy, significant decreases in urinary flow and compliance, presence of residual urine after voiding, voiding urgency and incontinence (). Obstructed bladder dysfunction secondary to BPH is a slow, progressive disease that is so strongly associated with human aging that it is an expected occurrence of the male aging process. Although the symptoms of BPH are usually not life threatening, they effect an extremely negative quality of life for men who suffer from them. However, many men delay seeking medical treatment for early BPH since bladder function can remain relatively normal as the hypertrophying bladder initially compensates for the progressive increase in urethral resistance caused by prostatic obstruction. The limited changes in micturition pressure and flow characteristics that occur during compensated function are not usually disabling enough to motivate seeking medical attention, which, often, is not sought until the symptoms become typical of advanced disease. Recent advances in detection methods enable identification of patients with significant BPH during compensation before the bladder becomes dysfunctional (decompensated). A more complete understanding of the disease processes that underlie the loss of bladder function associated with BPH might enable the development of treatments that better protect these early-stage BPH patients from the more debilitating aspects of the disease. This review updates the understanding of obstructive bladder dysfunction via the use of animal models.