中文摘要：

目的：基于睾丸扭转建立兔睾丸缺血再灌注损伤模型,探索缺血预处理对睾丸缺血再灌注损伤兔的睾酮水平及生精细胞凋亡的影响。方法：雄性新西兰大白兔15只,随机分为3组：A组（对照组）暴露右侧精索,不作缺血处理并关闭;B组（缺血再灌注组）使用无创血管夹夹闭右侧精索致睾丸缺血60 min,再灌注3 d;C组（预处理组）预先夹闭精索3次（缺血5 min/次＋灌注5 min/次）,余同B组。造模完成后,采用3%巴比妥钠麻醉兔后采集血液并分离血清,测定血清睾酮含量;随后分离睾丸组织,按照缺血侧及健侧分组后采用10%中性福尔马林固定组织,进行HE染色和TUNEL细胞凋亡检测。结果：术后A、C组体重比术前明显增加[（2.65±0.07）kg vs（2.45±0.07）kg、（3.03±0.11）kg vs（2.92±0.07）kg]（P均〈0.05）,B组手术前后体重没有变化[（3.05±0.07）kg vs（3.05±0.07）kg]（P〉0.05）。睾酮含量：手术前后A组没有明显差异[（139.59±9.39）ng/L vs（140.19±9.47）ng/L,P〉0.05];术后B、C组显著低于术前[（74.12±4.00）ng/L vs（148.06±3.31）ng/L、（94.76±3.13）ng/L vs（133.75±6.48）ng/L]和术后A组（P均〈0.01）。病理结果显示,与A组及B组健侧相比,B组缺血侧睾丸组织内大部分生精小管结构破坏,生精小管内各级生精细胞结构消失,可见凋亡的生精细胞,间质及管腔内有淡伊红色水肿液渗出,凋亡指数明显升高（P〈0.01）,Johnsen评分显著降低（P〈0.01）;与B组缺血侧相比,C组缺血侧睾丸组织基本恢复正常,凋亡指数明显降低（P〈0.01）,Johnsen评分显著增加（P〈0.01）。结论：缺血预处理明显缓减了睾丸缺血再灌注损伤后睾酮水平下降,并降低了细胞凋亡,为睾丸缺血再灌注损伤的临床治疗提供了潜在干预措施。

英文摘要：

Objective： To explore the effects of ischemic preconditioning on the level of serum testosterone （T） and apoptosis of spermatogenic cells in rabbits with testicnlar 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-minutenon-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 narco- tized 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 in- creased 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 ] rig/L, P 〈 0.01 ） as well as than the postoperative index in group A （ P 〈 0.01 ）. In compari- son 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