Abstract
AimsTo investigate the effect of a free radical scavenger (tempol) after relief of partial bladder outlet obstruction (pBOO) on bladder function in a rat model.MethodspBOO was induced in 50 eight-week-old female Sprague-Dawley rats and relieved 3 weeks later. The rats were divided randomly into 5 groups: sham-operated, tempol-treated for 1 week (Treat-1w) or 3 weeks (Treat-3w), and no treatment for 1 week (nonTreat-1w) or 3 weeks (nonTreat-3w). Awaken cystometrograms were obtained 1 or 3 weeks after relief according to the grouping. The bladders were isolated and weighed. H&E, Masson’s trichrome and TUNEL staining were used to analyze histological changes. The oxidative stress assessed using malondialdehyde. The expression of beta-3 adrenoreceptor was examined by Western blotting.ResultsThe tempol-treated groups exhibited a significant decrease in the number of non-voiding contractions per voiding cycle (nonTreat-1w vs. Treat-1w, 1.18±0.82 vs. 0.36±0.40, P = 0.010; nonTreat-3w vs. Treat-3w, 1.51±0.69 vs. 0.23±0.25, P = 0.002). The thickness and collagen fiber deposition of the detrusor muscle layer was significantly decreased in the treated groups. Apoptosis detected was mainly observed in the urothelial cell layer, although the rate of apoptosis was significantly decreased in the treated groups (48.9±3.36% vs. 32.7±11.10%, P = 0.024; 25.8±4.67% vs. 15.7±9.83%, P = 0.314). The tempol-treated groups showed significant decreases in the MDA concentrations at both 1 and 3 weeks after relief. The expression of the beta-3 adrenoreceptor was increased in the tempol-treated rats.ConclusionsIschemic reperfusion injury after relief of pBOO caused histological and functional changes in the bladder. Free radical scavenger treatment prevented this oxidative stress.
Highlights
Bladder outlet obstruction (BOO) occurs due to a variety of causes, including the posterior urothelial valve in children, urethral stricture in adults, and benign prostatic hyperplasia (BPH) in the elderly [1]
The tempol-treated groups exhibited a significant decrease in the number of non-voiding contractions per voiding cycle
Apoptosis detected was mainly observed in the urothelial cell layer, the rate of apoptosis was significantly decreased in the treated groups (48.9±3.36% vs. 32.7 ±11.10%, P = 0.024; 25.8±4.67% vs. 15.7±9.83%, P = 0.314)
Summary
Bladder outlet obstruction (BOO) occurs due to a variety of causes, including the posterior urothelial valve in children, urethral stricture in adults, and benign prostatic hyperplasia (BPH) in the elderly [1]. The most common cause in the clinic is BPH in older men, BOO may occur in women with several anatomical and/or functional etiologies, including pelvic organ prolapse, Skene’s gland cyst, primary bladder neck obstruction, and detrusor external sphincter dyssynergia [2]. In patients with severe degenerative bladder due to BOO, surgical treatment may temporarily exacerbate storage bladder dysfunction related to detrusor overactivity (DO) and even cause transient urgency and urgency urinary incontinence [4]. Developed urgency urinary incontinence after a HoLEP procedure has been reported in 7.1–44.0% of patients [5] This de novo urgency urinary incontinence causes significant stress and anxiety for the patients and for the surgeons, because it differs from post-operative complicated stress urinary incontinence. In a recent prospective study of persistent storage symptoms after successful relief of BOO, urodynamic DO was persistent in approximately 40% of the patients [6]
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