The influence of anti-ischemic therapy on the recovery of urinary bladder function after acute urinary retention

Introduction. Chronic ischemia is an important pathogenic factor of urination disorders in patients with benign prostatic hyperplasia (BPH). The aim of this study was to investigate the rationale for administering the drugs with anti-ischemic action in order to improve the urinary bladder function after acute urinary retention (AUR). Materials and methods. In our study, we investigated the effectiveness of anti-ischemic drugs approved for clinical trials (alpha-tocopherol, mexidol, pentoxyphyllinum and diltiazemum) on lowering the intensity of urinary bladder lesion and on the recovery of urination to a adequate level, in comparison with traditional alpha blocker therapy. We modelled AUR on 35 female rats and also used the case records of 90 patients with BPH accompanied by AUR. Results. According to the experimental studies, modelling of four-hour AUR was accompanied by significant damage of the detrusor smooth muscle mitochondria caused by reactive oxygen species production. These changes are cytotoxic and may stay behind urinary bladder dysfunction, due to the release of enzymes into the urine and the decrease of enzymatic activity in the detrusor cells. Anti-ischemic therapy preserves functional activity of smooth muscle mitochondria and prevents the excessive production of oxygen radicals. Consequently, there is a significant decrease of enzymeuria and maintenance of high enzymatic activity of in detrusor cells, especially creatine phosphokinase (CPK), which participates in energy supply for muscle contraction. The effectiveness of anti-ischemic therapy was comparable to protective action of doxazosin, an alpha-blocker; and several characteristics of the therapy were even better, in particular, with respect to CPK activity. Clinical results indicate that anti-ischemic therapy more effectively promotes the recovery of self-assisted urination, especially in patients with a larger residual urine volume and long anamnesis of the disease, in comparison with tamsulosin alpha-blocker therapy of patients with AUR. In addition, it prevents the damage of detrusor cells caused by AUR and more effectively lowers its negative effect on kidney function. Conclusion. Our results indicate the rationale for further research on the necessity of administering the anti-ischemic drugs in order to improve urination in patients with BPH.