Introduction. Prostatic hyperplasia (BPH) is one of the most common diseases of elderly and senile men. Its natural «evolution» leads to an increase in deformity disorders, gradual decompensation of the bladder and the progression of CKD. If the morphogenesis of BPH, as well as the patterns of adaptive and pathological restructuring of the lower urinary tract are described in the literature, then there is practically no evidence of adaptive processes in the prostate itself against the background of the growth of hyperplasia nodes. The purpose of the work: to study the features of morphological restructuring of prostate tissue and its vascular system in persons suffering from benign prostatic hyperplasia, with different levels of compensation for bladder function.
Material and methods. Autopsy material of 82 men aged 60-80 years was studied, divided into 4 groups: 25 men without GPH who died from causes unrelated to urological pathology; 25 men with GPH without clinical and morphological signs of bladder decompensation; 22 men with decompensated BPH, which is the main disease, where the immediate cause of death was chronic urinary retention, bilateral ureterohydronephrosis, CKD, uremia; 10 people who died from various causes, however, having a pathological diagnosis of BPH complicated by acute urinary retention. Fragments of the prostate gland were subjected to morphological examination. Histological sections were stained with hematoxylin-eosin, according to Mason and Hart, and also performed: overview microscopy, vascular morphometry and stereometry of the structural components of the prostate. In addition, an immunohistochemical study (IHC) was performed using mouse monoclonal antibodies to SMA.
The results of the study. The formation and progressive growth of prostate nodes in elderly and senile men leads to a compensatory restructuring of the tissue of this organ. Its manifestation is hypertrophy of the smooth muscles of the prostate and the restructuring of the arterial bed, which provides trophism to the overly developed smooth muscles of the stroma. Over time, sclerotic processes progress in the prostate tissue, which, on the one hand, have an inflammatory genesis, and, on the other, have a senile dyscirculatory character due to atherosclerosis of the extraorgan arteries and restructuring of the intraorgan arteries in connection with long-term arterial hypertension. As a result, the prostate gland becomes not only enlarged in volume due to hyperplasia nodes, but also rigid due to fibrosis, which, along with hypertrophy of the smooth muscle component of the stroma, contributes to a further increase in resistance to urine outflow.
An increase in the size of nodes, inflammatory edema of the organ, its sclerosis and petrification, as well as progressive reduction of the arterial bed, lead to the development of venous hyperemia and lymph circulation disorders, being a morphological prerequisite for acute urinary retention.
Conclusion. In GPH, compensatory and adaptive processes occur not only in the detrusor, but also in the prostate gland, as well as its vascular bed. At the same time, aimed at ensuring the normal functioning of the organ in conditions of formation of hyperplastic nodes, they eventually lead to its pathological restructuring, themselves becoming the cause of impaired urine outflow, predetermining the dynamics of the disease and the occurrence of its complications.

Keywords: stroma, vascular bed, prostate hyperplasia, decompensation, compensation, acute urinary retention