Investigation the effects of nimodipine on experimental testicular torsion/detorsion model

Introduction: Testicular torsion (TT) is one of the most significant causes of acute scrotum, occurring as a result of twisting the spermatic cord and its contents around themselves. Following TT ischemic injury, and after detorsion reperfusion injury may occure. Numerous studies have been conducted to prevent ischemia and reperfusion (I/R) injury. In the literature, there are studies investigating the effects of nimodipine, a calcium channel blocker, on I/R injury in the ovaries and liver, but no study has been found examining its effects on TT at the ultrastructural level. In our study, investigation the potential therapeutic effects of nimodipine on experimental testicular torsion/detorsion model was aimed. Materials and Methods: Forty male Wistar-Albino rats, weighing 250-300 grams, were divided into 5 groups (n=8); the Sham group, testicular torsion group (TT), testicular torsion/detorsion group (TT/D), testicular torsion + nimodipine group (TT/N), and testicular torsion/detorsion + nimodipine group (TT/D/N). In blood samples collected from the rats before sacrification SOD activity, serum MDA, and testosterone analyses were performed. The obtained testicular tissue samples were prepared for light and electron microscopic examinations. Additionally, the expressions of caspase-3 as an apoptotic marker, and TNF-α as an inflammation marker, were investigated in testicular tissue sections using immunohistochemical methods. Results: Under light microscopy, in the TT and TT/D groups thickening in the tunica albuginea, degenerative, lytic, and apoptotic changes in the seminiferous tubules, edema and hemorrhage in the interstitial area were observed. At the electron microscopic level in the TT and TT/D groups thickening and irregularities in the basal lamina and membrana propria, detachment of the seminiferous tubule epithelium from the basal lamina, widening and the presence of apoptotic bodies in the intercellular spaces, degenerative change in Sertoli cells, disruptions in the structure of occluding junctions, enlargements of mitochondria and endoplasmic reticulum cisternae, and increases in the number of lipid droplets and lysosomes were observed. In spermatogenic series cells, enlargements of mitochondria and endoplasmic reticulum cisternae were also noted. In the interstitial area, the presence of extravascular erythrocytes, widening of intercellular spaces, degenerative changes in the structure of Leydig cells were observed. An increase in inflammatory cells, particularly in the T/D group, was noticeable. In the groups treated with nimodipine (TT/N and TT/D/N), a near normal morphology was observed at both light and electron microscopic levels. Increased caspase-3 and TNF-α immunoreactivities were observed in the TT and TT/D groups, while decreases were noted in the TT/N and TT/D/N groups. The TT and TT/D groups showed increases in serum MDA concentrations and decreases in SOD activity and serum testosterone concentrations. In the TT/N and TT/D/N groups, statistically significant increases in SOD activity and serum testosterone levels were observed compared to the damage groups, along with decreases in serum MDA concentrations. Conclusion: When all the findings are considered together; it was concluded that nimodipine treatment demonstrated therapeutic effects on the structural changes and biochemical impairments observed in the TT and TT/D groups, suggesting that it could be used as an alternative therapeutic agent in testicular I/R injury. However, further experimental and clinical studies are needed to obtain more information about the molecular mechanisms of this treatment and to make dose and duration adjustments. Keywords: Testicular torsion/detorsion, nimodipine, calcium channel blocker.