Correspondence

Abstract

In the August 2004 issue of Journal of Anatomy, Kong and colleagues reported that unilateral vasectomy in rabbits resulted in ipsilateral (‘vasectomy-induced’) damage to spermatogenesis – most severely at 10 days (in all testes), and less severe in about half the testes at 6 and 12 months. This testis-damaging effect of vasectomy contrasts with their previous results in the rhesus monkey in which the testes showed no such damage. Because of an interest in the keratinoid tough quality of mammalian sperm, and how they are disposed of after vasectomy (and because of the importance of vasectomy in humans), in the mid-1970s I studied this question in the rhesus monkey, hamster, rat and rabbit (Bedford, 1976). After vasectomy in these animals spermatogenesis usually continued normally. However, sperm accumulation brought a rupture at one or more focal points in the lower epididymis or vas deferens within a few weeks in the monkey, hamster and rat – but with the rabbit as a notable exception. Apparently because of the relatively elastic distensible quality of the lower duct in the rabbit, the accumulating sperm simply produced an increasing distension or dilatation of its vas deferens and cauda epididymidis, with little or no change in the upper epididymis. As this distal accumulation and distension progressed over the next months the intact rabbit cauda epididymdis and vas became relatively huge until, beginning at about 6 months after vasectomy, some ducts ruptured focally and formed granulomata (sperm disposal sites). In order to quantify this situation, Moore & Bedford (1978) counted the sperm total accumulating at 1, 2, 4 and 6 months after vasectomy. Somewhat surprisingly even to us, after vasectomy the number of spermatozoa accumulating in the distensible epididymis/vas at each time period was equivalent to the total that would be produced by a normal testis over the same time period – in other words, after vasectomy spermatogenesis had continued at a normal rate over a 6-month period in the rabbit. In both our studies the rabbit testicular weights (one sensitive indicator of function) were similar on the vasectomized and control sides, with the notable exception of occasional animals in which a granuloma had formed high in the epididymis. Regrettably, the conclusion of Kong et al. that vasectomy in the rabbit soon results in testicular damage is incorrect, and the pattern of their own results reinforces this view. The fact that the greatest testicular damage was seen in their study after only 10 days, when sperm accumulation is minimal, suggests that the damage may have resulted not from vasectomy per se but from local trauma or inflammation. This will occur quite readily after exposure of the vas deferens by incision of the skin and processus vaginalis of the rabbit scrotum, rather than via one small central incision in the high inguinal region. Since Kong et al. (2004) quote Bedford (1976) in explaining the testicular damage, it is puzzling that they do not comment also on the very different pattern of the respective results.