Functional morphology of the bladder and its vascular system in relation to age changes and evolution of BPH

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Abstract

Introduction. The increase in the proportion of people with various urinary disorders, which are based on anatomical and functional bladder remodeling due to aging, is currently un-deniable. This problem becomes more relevant due to the elevation in life expectancy. At the same time, the features of bladder remodeling, in particular, the structural changes of its vascular bed, are still practically not described in the literature. In men, the lower urinary tract undergoes additional transformation associated with age due to bladder outlet obstruction caused by benign prostatic hyperplasia (BPH). Despite the long history of studying BPH, the morphological basics of its evolution have not yet been fully elucidated, including the development of lower urinary tract decompensation and, in particular, the role of vascular changes. In addition, structural re-modeling of the bladder muscles in BPH is formed in those with pre-existing age-related changes in both the detrusor and its vascular system, which cannot but influence the dynamics of disease progression.

Aim. To study the structural changes of detrusor and its vascular bed associated with age, and to establish the role of their patterns in patients with BPH.

Materials and methods. The material was a specimen of the bladder wall obtained dur-ing: a) autopsies of 35 men aged 60–80 years who died from diseases not related to urological or cardiovascular pathology; b) autopsies of 35 men aged 60–80 years who had BPH without blad-der decompensation; c) intraoperative biopsies of 25 men of the same age who undergone surgical treatment for chronic urinary retention (postvoid residual volume of more than 300 ml), bilateral hydronephrosis, as complications of BPH. As a control, we used the specimens obtained from 20 males aged 20–30 years who died as a result of violence.

Histological sections of the bladder wall were stained with hematoxylin-eosin, according to Mason and Hart. Standard microscopy and stereometry of detrusor structural components and morphometry of the urinary bladder vessels were performed using a special ocular insert with 100 equidistant points. During morphometric examination of the vascular bed the thickness of the middle layer of arteries wall (tunica media) was measured, as well as a thickness of the entire wall of the veins in microns. In addition, a Schiff test and Immunohistochemistry (IHC) of these histological sections were performed. The IHC was evaluated using a semi-quantitative method, taking into account the degree of staining in 10 fields of vision (×200).

The digital material was processed with the STATISTICA program using the Student's t-test. The distribution of the obtained data corresponded to normal. The data were considered re-liable if the probability of making error did not exceed 5% (p<0.05).

Results and discussion. In the course of natural aging, a structural remodeling of bladder vascular bed was observed, from the development of atherosclerosis of extra-organ arteries to restructuring of intra-organ arteries due to arterial hypertension. The progression of angiopathy leads to the development of chronic detrusor ischemia, which initiates the formation of focal at-rophy of the smooth muscles, destructive changes in the elastic fibers, neurodegeneration and stroma sclerosis. A long-term BPH leads to compensatory detrusor remodeling with hypertrophy of previously unchanged areas. At the same time, age-related atrophic and sclerotic changes in smooth muscles are accompanied with hypertrophy of individual areas of the bladder detrusor.

To maintain adequate blood supply to hypertrophied detrusor areas in the arterial and venous bladder vessels, a complex of myogenic structures is formed that can regulate blood circulation, making it dependent on the energy consumption of specific areas. However, progressive age-related changes in the arteries and veins eventually lead to an increase in chronic hypoxia, impaired nervous regulation and vascular dystonia, increased blood vessels sclerosis and hyalinosis, and sclerosis of intravascular myogenic structures with loss of their function of blood flow regulation, as well as the development of vein thrombosis. As a result, increasing vascular decom-pensation in patients with bladder outlet obstruction results in bladder ischemia and accelerates the decompensation of the lower urinary tract.

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About the authors

I. S. Shormanov

Yaroslavl State Medical University of the Ministry of Health of the Russian Federation

Author for correspondence.
Email: i-s-shormanov@yandex.ru

Ph.D., MD, Professor, Head of the Department of the Urology and Nephrology

Russian Federation, Yaroslavl

S. V. Kulikov

Yaroslavl State Medical University of the Ministry of Health of the Russian Federation

Email: kulikov268@yandex.ru

Ph.D., MD, Associate Professor, Head of the Department of Pathology

Russian Federation, Yaroslavl

A. S. Soloviev

Yaroslavl State Medical University of the Ministry of Health of the Russian Federation

Email: a-s-soloviev89@yandex.ru

Ph.D., Associate Professor of the Department of Urology with Nephrology

Russian Federation, Yaroslavl

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2. Fig.1. IGH. Hypertrophy of the middle shell of the large intra-organ artery of the bladder with high expression of smooth muscle actin a-SMA in the smooth muscles of the vessel and detrusor myocytes (shown by arrow) with compensated prostatic hyperplasia and m

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3. Fig. 2. IGH. hypertrophy of smooth muscles of the wall of a large bladder vein with high expression of smooth muscle actin a-SMA in compensated prostatic hyperplasia

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4. Fig. 3. Overview microscopy. Hypertrophy of detrusor smooth muscle cells in compensated prostatic hyperplasia

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5. Fig. 4. IGH. Weak expression of S100 protein in detrusor nerve fibers in compensated prostatic hyperplasia

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6. Fig. 5. Coloring of elastic fibers. The bundle of intimate muscles of the small artery (shown by the arrow), located between the sheets of the internal elastic membrane with compensated prostatic hyperplasia

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7. Fig. 6. Overview microscopy. Musculoelastic sphincter at the mouth of the middle artery, represented by two lobes (shown by an arrow) with compensated prostatic hyperplasia

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8. Fig. 7. Coloration of collagen fibers. A muscle roller in the wall of a large vein protruding into its lumen with compensated prostatic hyperplasia

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9. Fig. 8. Survey microscopy. Gross sclerosis and hyalinosis of detrusor with smooth muscle atrophy in decompensated prostatic hyperplasia

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10. Fig. 9. Coloring of elastic fibers. Incorrect configuration of the lumen and uneven folding of the internal elastic membrane of the small artery of the bladder in decompensated prostatic hyperplasia

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11. Fig. 10. Survey microscopy. Hyalinosis of the musculoelastic sphincter and sclerosis of the wall of the middle artery in decompensated prostatic hyperplasia

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