Abstract
Objective of the study was to analyze the particulars of morphofunctional changes in pelvic organs under conditions of stress urinary incontinence and experimental vaginal prolapse. Materials and methods. The experimental studies were conducted on 50 sexually mature white female rats divided into three groups. The first control group consisted of intact animals; the 2-nd group consisted of animals with replicated stress urinary incontinence model; and the 3-rd group consisted of animals with a combined model, in which, after replication of the stress urinary incontinence model, the vaginal vault fixation to sacro-uterine ligaments was broken, thus causing vaginal prolapse. After withdrawal of animals from the experiment, histological studies of bladder, urethra and vulva were carried out. Study results. After replication of the stress urinary incontinence and vaginal prolapse model, the destructive processes in the mucous membranes of the bladder, urethra, and vulva were developing, the volume of connective tissue in muscle membranes was increasing, the collagen fibers were thickening, and one could observe changes thereof with manifestations of destruction within a 30-day period. A combination of these processes led to an alteration of histoarchitectonics and the muscle ratio and connective tissues in membranes covering the study organs in both groups. Pathological changes accompanied by structural rebuild of bladder, urethra, and vulva tissues were more pronounced in the combined model. Conclusions. Replication of the stress urinary incontinence model in the bladder of female rats caused an overactive state of the above, while the muscle membranes of urethra and vulva became moderately atonic. The combined stress urinary incontinence and vaginal prolapse model used by us was successfully replicated in all animals of the experimental group, which was confirmed by morphofunctional changes in the bladder, urethra and vulva tissues. Functional changes dominated in animals with the stress urinary incontinence model. The animals with a combined stress urinary incontinence and vaginal prolapse model presented with functional changes predominantly observed on day 14, and changes in the histoarchitectonics of the study organs on day 30. Replication of the combined stress urinary incontinence + vaginal prolapse model resulted in swelling of the vulva tissues, accompanied by growth and consolidation of collagen fiber bundles, muscular and mucosal membranes atrophy, and decreased quantity of microcirculatory bed vessels. Pathological changes in structural elements of the vulva after application of the combined model suggested a trophic disturbance, which was confirmed by a decrease in the density of capillaries by 34.24% and fibrosis of arteriolar membranes.
Highlights
At the present time, difficulties in solving the problem of etiology and pathogenesis of the genital prolapse persist
A significant number of genital prolapse cases in women is caused by systemic changes in connective tissue, trauma of the connective apparatus of the genital organs and pelvic floor fasciae, microcirculatory and trophic disorders, and the deficiency of estrogen
Deterministic defect in molecular structure of the collagen resulting in a decrease of the strength of fixing apparatus and fasciae of the pelvic floor is considered a factor of risk for development of the genital prolapse [9]
Summary
Difficulties in solving the problem of etiology and pathogenesis of the genital prolapse persist. A significant number of genital prolapse cases in women is caused by systemic changes in connective tissue, trauma of the connective apparatus of the genital organs and pelvic floor fasciae, microcirculatory and trophic disorders (especially in elderly and hyposthenia persons), and the deficiency of estrogen. This is so-called “fatigue-driven” prolapse [2, 3]. Estrogen deficiency is believed to be the most important factor that influences metabolic processes in the connective tissue and chemical composition of the intercellular media This was manifested by deceleration of the processes of collagen synthesis and decreased elasticity of the connective tissue [7, 8]. Deterministic defect in molecular structure of the collagen resulting in a decrease of the strength of fixing apparatus and fasciae of the pelvic floor is considered a factor of risk for development of the genital prolapse [9]
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