[Effects of ischemic preconditioning on the serum testosterone level and spermatogenic cell apoptosis in rabbits with testicular ischemia-reperfusion].

Objective: To explore the effects of ischemic preconditioning on the level of serum testosterone (T) and apoptosis of spermatogenic cells in rabbits with testicular ischemia-reperfusion injury induced by testicular torsion.
Methods: A total of 15 New Zealand male rabbits were randomly divided into groups A (control), B (ischemia-reperfusion), and C (ischemic preconditioning). The animals of group A were subjected to exposure of the right spermatic cord without ischemia, those of group B received 60-minute non-invasive occlusion of the right spermatic cord followed by 3 days of reperfusion, and those of group C underwent 5-minute occlusion plus 5-minute reperfusion of the right spermatic cord followed by the same procedure as that for group B. Then the rabbits were narcotized with 3% barbital sodium, the whole blood collected for examination of the serum T content and the testis tissues obtained from both the ischemic and healthy sides for HE and TUNEL staining.
Results: After operation, the body weight was significantly increased as compared with the baseline in groups A (［2.65±0.07］ vs ［2.45±0.07］ kg, P<0.05) and C (［3.03±0.11］ vs ［2.92±0.07］ kg, P<0.05), but not in group B (［3.05±0.07］ vs ［3.05±0.07］ kg, P>0.05). The serum T level showed no statistically significant difference in group A before and after operation (［139.59±9.39］ vs ［140.19±9.47］ ng/L, P>0.05), but was remarkably lower after operation than the baseline in groups B ［148.06±3.31］ vs ［74.12±4.00］ ng/L, P<0.01) and C (［133.75±6.48］ vs［94.76±3.13］ ng/L, P<0.01) as well as than the postoperative index in group A (P<0.01). In comparison with group A and the healthy side of group B, the testis tissue of the ischemic side in group B exhibited structural damage of most of the seminiferous tubules with disappearance of spermatogenic cell structures, apoptosis of spermatogenic cells, and exudation of light-eosin edema fluid in the mesenchyme and lumen, with a markedly increased apoptosis index (P<0.01) and a significantly decreased Johsen's score (P<0.01). Compared with ischemic side of group B, The testis tissue of the ischemic side in group C was restored to normal as compared with that in group B, with a dramatically decreased apoptosis index (P<0.01) and a remarkably increased Johnsen's score (P<0.01).
Conclusions: Ischemic preconditioning can raise the decreased serum T level and reduce the apoptosis of spermatogenic cells in rabbits with testicular ischemia-reperfusion injury, which could be applied as a potential option for the clinical treatment of testicular ischemia-reperfusion injury.