After surgical correction of testicular torsion, up to 68% of ipsilateral testes undergo atrophy due to ischemia-reperfusion injury (IRI). Recent studies have shown that dexmedetomidine (Dex) alleviates IRI in various vital organs. However, those studies evaluated its protective effect on short-term reperfusion.
We aimed to investigate whether Dex has a long-term protective effect against testicular injury after IRI.
A total of 24 New Zealand white rabbits were randomly divided into three groups (n = 8/group): the control group (saline-infused rabbits without IRI), the IRI group (saline-injected rabbits with IRI), and the Dex group (Dex-injected rabbits with IRI). The spermatic cord of rabbits in IRI and Dex groups was ligated for 4 h, and 1 h before reperfusion, Dex was administered intraperitoneally at a dose of 50 μg/kg body weight in group Dex, whereas saline was administered at the same dose to the IRI and control groups. Rabbits were kept alive for 4 weeks post reperfusion, then the testes were harvested, and the rabbits were euthanized.
Four weeks post reperfusion, testicular volumes of the affected side decreased considerably in the IRI and Dex groups compared to the control group, with no significant difference between the IRI and Dex groups. Compared to the control group, the Johnson score and the mean seminiferous tubular diameters were significantly decreased in the IRI and Dex groups, but no significant differences were observed after administration of Dex. There were no significant differences in malondialdehyde and superoxide dismutase levels between the groups treated with and without Dex.
Dex administration 3 h after ischemia and 1 h before reperfusion did not demonstrate a significant protective effect against testicular injury 4 weeks after IRI in rabbits. Further research is needed to confirm the potential therapeutic effects of Dex by varying the experimental conditions.