Ultrastructural Changes in Smooth Muscle Cells of the Urinary Bladder Due to Benign Prostatic Hyperplasia

Abstract

The objective: to evaluate the ultrastructural changes of smooth muscle cells (SMCs) of the urinary bladder (UB) in benign prostatic hyperplasia (BPH). Materials and methods. 70 patients with BPH were selected by the random sampling (average age – 67.94±7.42 years old). The patients were divided into three groups according to clinical manifestations. The first group included 20 patients with accumulation symptoms: disease duration – 4±1.8 years, I-PSS – 16±4.5 points, Qmax – 15.8±2.4 ml/s, Qave – 12.8±2.8 ml/s, absence of residual urine (RU). The second group included 20 patients with incomplete emptying of UB: disease duration – 5.8±3.5 years, I-PSS – 26±3.9 points, Qmax – 10.8±2.5 ml/s, Qave – 4.4±1.4 ml/s, volume of RU – 150.1±80.8 ml. The third group included 30 patients with cystostomy: disease duration – 10.6±3.3 years, before cystostomy: I-PSS – 33.1±1.88 points, volume of RU – 1093.3±458.8 ml. The study of the ultrastructure of UB myocytes was carried out by standard methods of electron microscopy. Results. There were the ultrastructural changes of the SMCs in patients with BPH in the first group in the compensation stage UB, the hypertrophied smooth muscle cells with little changed ultrastructure were determined. In patients with BPH of the second group in the subcompensation stage of UB, hypertrophied SMCs with slightly changed ultrastructure and SMCs with more changed ultrastructure were found, and single dystrophic SMCs were also established, the mitochondria of which were distinguished by focal or total matrix lysis, destruction of cristae, and discomplexation of organelles. Single necrobiotically altered SMCs were found, which are probably subject to elimination. There were cells the ultrastructure of which corresponds to the newly formed SMCs, which indicates the preservation of regenerative potential. The ultrastructural changes of SMCs were revealed in BPH patients of the third group in the stage of CM decompensation: multiple dystrophically changed “dark” and necrobiotically changed “light” SMCs, which are likely to be eliminated. Conclusions. Due to the untimely elimination of the obstruction there is a persistent disorder of the evacuator function of the urinary bladder and, as a result, incomplete emptying, violation of the urodynamics of the upper urinary tract, persistence of urinary infection, and in advanced cases – the development of chronic kidney failure. The formation of clinical symptoms occurs due to the complex process of pathomorphological changes in CM. At the stage of UB compensation with BPH, the SMCs are hypertrophied with little changed ultrastructure, which ensures the contractile capacity of the detrusor. At the stage of subcompensation of CM the hypertrophied SMCs with little changed ultrastructure still predominate, but dystrophically changed “dark” and necrobiotic “light” cells appear. At the stage of CM decompensation, the specific weight of dystrophically changed “dark” SMCs and necrobiotic “light” SMCs increases significantly. At the same time, the absence of “young” SMCs indicates the exhaustion of the regenerative potential and the irreversibility of the ultrastructural changes of the UB.