摘要
By utilizing the rabbit model, previous studies have found good evidence indicating that vasectomy-induced spermatogenic damage is pressure-mediated： the damage occurs when the occluded reproductive tract is unable to accommodate additional spermatozoa produced by the testis. More studies with the more commonly used rat model have shown, however, controversial results on whether and why the damage occurs. In this study, 12 mature male Sprague-Dawley rats were subjected to unilateral vasectomy： double ligation （without severing） of the vas deferens exposed via a small inguinal incision; 37 days after the operation, the testes, epididymides, vasa deferentia （juxta-epididymal segments）, and sperm granulomas （at the vasectomy site） were removed to obtain methacrylate resin-embedded sections and morphometric studies carried out with light microscopy. Marked spermatogenic damage with spermatids and spermatocytes depleted in the seminiferous epithelium in 43% of the seminiferous tubule profiles was demonstrated in 5 of the 12 testes on the vasectomized side, and the damage was associated with smaller or absent sperm granulomas; in the other 7 testes with essentially normal spermatogenesis, there was an increase （by 111% on average） in the volume of the tubule lumen, associated with larger granulomas or granulomas containing more spermatozoa. There was an overall increase （by 66%） in the thickness of the rete testis in the 12 testes; the epididymis or vas deferens showed no distension. It seems therefore that the spermatogenic damage induced by vasectomy in rats is pressure-mediated as well, and that variation in the damage depends mainly on the postoperative development of the sperm granuloma.
By utilizing the rabbit model, previous studies have found good evidence indicating that vasectomy-induced spermatogenic damage is pressure-mediated： the damage occurs when the occluded reproductive tract is unable to accommodate additional spermatozoa produced by the testis. More studies with the more commonly used rat model have shown, however, controversial results on whether and why the damage occurs. In this study, 12 mature male Sprague-Dawley rats were subjected to unilateral vasectomy： double ligation （without severing） of the vas deferens exposed via a small inguinal incision; 37 days after the operation, the testes, epididymides, vasa deferentia （juxta-epididymal segments）, and sperm granulomas （at the vasectomy site） were removed to obtain methacrylate resin-embedded sections and morphometric studies carried out with light microscopy. Marked spermatogenic damage with spermatids and spermatocytes depleted in the seminiferous epithelium in 43% of the seminiferous tubule profiles was demonstrated in 5 of the 12 testes on the vasectomized side, and the damage was associated with smaller or absent sperm granulomas; in the other 7 testes with essentially normal spermatogenesis, there was an increase （by 111% on average） in the volume of the tubule lumen, associated with larger granulomas or granulomas containing more spermatozoa. There was an overall increase （by 66%） in the thickness of the rete testis in the 12 testes; the epididymis or vas deferens showed no distension. It seems therefore that the spermatogenic damage induced by vasectomy in rats is pressure-mediated as well, and that variation in the damage depends mainly on the postoperative development of the sperm granuloma.
