LEYDIG-CELL FUNCTION AFTER EXPERIMENTAL TESTICULAR TORSION DESPITE LOSS OF SPERMATOGENESIS

Little is known about specific testicular cell responses to periods of testicular torsion. In particular, the steroidogenic capacity of Leyd ig cells in the post-torsion testis is unknown. Male Sprague-Dawley ra ts (450-550 g) underwent no torsion (control) or a 720 degrees unilate ral testicular torsion for either 0 (sham), or 1 or 2 hours. Such tors ions have previously been shown to cause progressive damage to the rat testis. One, 15, or 30 days after torsion repair all animals (n = 5-1 0/group) were prepared for testicular venipuncture and intravenous inf usion of ovine luteinizing hormone (LH) via the femoral vein. Testicul ar venous blood was collected directly from the surface of the testis both 5 minutes prior to and 90 minutes after infusion of predetermined ED(50) (0.1 mu g) or ED(100) (0.5 mu g) doses of LH. Testicular venou s serum (TVS) was assayed for testosterone (T) by radioimmunoassay. Co ntrol animal TVS T concentrations before LH infusion and 90 minutes af ter ED(50) and ED(100) LH stimulation were 103 +/- 25, 621 +/- 103, an d 1,055 +/- 140 ng/ml, respectively. Testes having experienced a 1-hou r torsion did not have a significantly (P < 0.05) reduced capacity to respond to ED(50) and ED(100) stimulation at either 15 and 30 days aft er the torsion. Testes having experienced a 2-hour torsion did have si gnificantly reduced (P < 0.05) ED(50) responses at both 1 hour and 30 days after torsion repair. More remarkably, significant steroidogenic reserve was still present in testes after torsion, which in previous s tudies had been shown to have permanent loss of spermatogenesis. The f unctional survival of Leydig cells bodes well for the potential to fin d medical treatments that will aid in the survival of the torsed testi s.