Introduction. In conditions of long-term infravesical obstruction caused by prostate hyperplasia (РН), 15-30% of patients eventually experience decompensation of detrusor function. At the same time, the details of the adaptive transformation of the vascular bed of the bladder, as well as its correlation with the structural remodeling of this organ, which determine the decompensation of the lower urinary tract in conditions of chronic urinary retention, are still unclear.

Aim. To study the role of vascular and age-related factors in the depletion of the compensatory reserve of detrusor in long-term РН in elderly and senile people.

Material nd meathods. Autopsy material from 25 men who did not have urological pathology, from 25 men who had РН without signs of decompensation of the bladder and biopsy material from 25 patients operated on for РН in the decompensation stage were examined. The age of all persons ranged from 60 to 80 years. Control – 10 men aged 20-30 years, who died as a result of injuries. Histological sections of the areas of the bladder were stained with hematoxylin-eosin, according to Mason and Hart.

Results. In conditions of long-term РН, the functioning of a locally hypertrophic detrusor occurs against the background of age-related atrophic-sclerotic changes in it, the cause of which is: atherosclerosis of large arteries, as well as hyalinosis of small arteries and arterioles, characteristic of arterial hypertension.The «working capacity» of the bladder under these conditions is provided by the activity of regulatory muscle formations in the arterial and venous basins, with the help of which the necessary level of oxygenation is achieved. However, progressive age-related changes in the cardiovascular system over time lead to an increase in chronic ischemia. Sclerotic changes develop in the regulatory structures of the arteries and veins. As a result, there is a gross diffuse sclerosis of the detrusor with atrophy of the muscle fibers.

Conclusions. Decompensation of detrusor in РН is a consequence of earlier vascular decompensation, the morphological markers of which are: arteriosclerosis, phlebosclerosis and sclerosis of regulatory structures.