Model of Hypogonadism by Method of Testicular Ischemization and its Morphological Substantiation

Abstract

This study is devoted to the morphological substantiation of the model of male hypogonadism and establishing the effectiveness of its replacement therapy using morphological methods. Material and methods. 5 groups of adult male Wistar rats (4 individuals each) were studied. Four groups of rats were experimental. Under anesthesia, the left and right spermatic cords with the vascular bundle were tied with a temporary ligature, inducing hypogonadism. In the first two experimental groups of rats, the ligature was applied for 30 and 60 minutes (respectively). Animals in the other two experimental groups received replacement therapy by administering kisspeptin K6. Animals of the third experimental group began to receive kisspeptin a few minutes after restoration of blood flow in the testicle (ex tempore), and rats of the fourth group - after 3 days. The duration of replacement therapy is 7 days. In histological sections of the right and left testicle (n = 8), the number of viable and dying interstitial endocrine cells was counted (under the control of an immunohistochemical reaction with caspase 3), the percentage of these types of cells from their total number was calculated, and the area of viable endocrinocytes was determined. Testosterone levels were determined in the blood of animals of all groups. The significance of differences in the median, upper and lower quartiles of the compared parameters was determined using the nonparametric Mann–Whitney test. Results. It has been established that the modeling of male hypogonadism by applying a double-sided ligature to the vessels of the spermatic cord for 60 minutes and the animals experiencing it for the next 10 days induces pronounced reactive changes and the death of some interstitial cells, inhibition and cessation of spermatogenesis. Kisspeptin KS6, administered ex tempore and regularly after acute ischemia, has a protective effect on interstitial endocrinocytes and testicular spermatogenic cells, including anti-apoptotic, restoring spermatogenesis, probably realized through the activation of the central links of the hypothalamic-pituitary-testicular axis.