The pathogenetic importance of chronic ischemia of the pelvic organs in the development of benign prostate hyperplasia (BPH) and concurrent bladder dysfunction was investigated in chronic experiments on 18 male rats. Chronic ischemia was induced by the contraction of the inferior vena cava (1st series). In the second series BPH was induced with the use of androgen therapy (once a week Sustanon for 1 month). Intact rats were used as controls. In both series the development of BPH was evident. In the group of androgen therapy a prominent glandular form of the BPH was developed, in the group with chronic ischemia – stromalglandular form. In the experiments with chronic ischemia a 3-times less intramural blood supply was the registered event in the prostate and urinary bladder, leading to the development of detrusor hyperactivity without the signs of infravesical obstruction. Androgen-induced BPH led to the increase in prostate blood flow; at that bladder blood supply was firstly decreased and then increased over the initial rate. Hormonal status investigations showed that in group of chronic ischemia induced BPH testosterone level was normal, as were the level of estradiol and insulin in blood with concurrent modest increase of the testosterone concentration in the prostate tissues without any changes in tissue levels of other hormones. In the group of androgen therapy BPH development was accompanied with drastic increase of the androgen and estradiol levels in blood and prostate tissues. This enabled us to make a conclusion, that androgen stimulation and chronic ischemia of prostate are two independent pathogenic factors of the BPH development.
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