Features of compensatory and adaptive reactions of the vascular bed of the bladder of elderly and senile men with prostatic hyperplasia

Abstract

BACKGROUND: Bladder outlet obstruction caused by prostatic hyperplasia eventually leads to detrusor working hypertrophy, and its development is impossible without synchronous remodeling of its vascular bed. Taking into account the age-associated nature of the disease, bladder transformation occurs following involutive structural changes of both the organ and its vascular system due to natural aging. To date, morphological features of compensatory reactions of the vascular bed, taking into account background age-related changes in the bladder wall, is not fully disclosed.
 AIM: To investigate the structural transformations of the bladder and its vascular bed in elderly and senile persons with prostatic hyperplasia and to determine the significance of vascular restructuring in providing compensatory detrusor hypertrophy.
 MATERIALS AND METHODS: Autopsy material from 35 men aged 6080 years who died from diseases not related to urological and cardiovascular pathology was examined, as well as those from 25 men of the same age who had prostatic hyperplasia without signs of bladder decompensation. The control group included 15 men aged 2030 years who died as a result of injuries. A complex of histological, morphometric and immunohistochemical methods was used
 RESULTS: In patients with prostatic hyperplasia, there is a violation of the histoarchitectonics of the bladder, which is expressed in the development of focal detrusor hypertrophy, layering on the existing involutive changes, which are characterized by the atrophy of muscle fibers, sclerosis of the intermuscular stroma, defragmentation of the elastic frame, and neurodegenerative processes. A similar state of the detrusor is caused by sclerosis and hyalinosis of small arteries and arterioles, hypertrophy and hyperelastosis of large arteries associated with arterial hypertension, combined with atherosclerosis of extraorganic arteries. Moreover, a complex is formed in the vascular basin of the bladder that can regulate blood transport in conditions of increasing chronic ischemia and provide a normal blood supply to the preserved parts of the detrusor that can undergo hypertrophy with an increase in functional impairment. These structures include intimate muscles, muscular elastic sphincters, polypoid cushions of the conti arteries, muscle couplings, muscle rollers, and vein valves.
 CONCLUSIONS: Structural changes in the bladder are characterized by a combination of focal detrusor atrophy resulting from angiosclerosis and development of hypertrophy of preserved areas with an increase in functional load. The hypertrophic potential of the detrusor is attributed to vascular regulatory structures.