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Male germ cells are quite sensitive to interruption in blood flow. Eight weeks after subjection to 45 minutes of testicular ischemia, the spermatogenic epithelium of the rat remains significantly damaged, though other cell types are well preserved. The authors evaluated the testicular recovery of the rats at 8 and 72 weeks after the 45‐minute period of warm ischemia. Twenty‐eight rats were studied: 14 underwent 45 minutes of total left testicular ischemia; 14 received no treatment. Four rats from each group were necropsied at S weeks to document the ischemic injury. At 72 weeks, the 18 surviving rats were necropsied to evaluate the long‐term outcome of the treatment. At 8 weeks, significant left testicular injury was documented. However, at 72 weeks there was no difference in testicular weight or sperm head count between the groups: in all 36 testicles, the repopulation index was 1.00, the epididymal index was 3+, the modified Johnsen index was 14, and the spermatic cord score was 7 (all are maximum obtainable scores). Neither contralateral orchiopathy nor injury to spermatic cord structures was observed. Our work shows that ischemia‐induced testicular injury is fully reversible with time in this model.
Male germ cells are quite sensitive to interruption in blood flow. Eight weeks after subjection to 45 minutes of testicular ischemia, the spermatogenic epithelium of the rat remains significantly damaged, though other cell types are well preserved. The authors evaluated the testicular recovery of the rats at 8 and 72 weeks after the 45‐minute period of warm ischemia. Twenty‐eight rats were studied: 14 underwent 45 minutes of total left testicular ischemia; 14 received no treatment. Four rats from each group were necropsied at S weeks to document the ischemic injury. At 72 weeks, the 18 surviving rats were necropsied to evaluate the long‐term outcome of the treatment. At 8 weeks, significant left testicular injury was documented. However, at 72 weeks there was no difference in testicular weight or sperm head count between the groups: in all 36 testicles, the repopulation index was 1.00, the epididymal index was 3+, the modified Johnsen index was 14, and the spermatic cord score was 7 (all are maximum obtainable scores). Neither contralateral orchiopathy nor injury to spermatic cord structures was observed. Our work shows that ischemia‐induced testicular injury is fully reversible with time in this model.
Unilateral spermatic cord torsion results in contralateral degeneration and reduced fertility in the prepubertal male rat. This study was conducted to investigate the use of immunosuppression with cyclosporine and prednisone to prevent these untoward effects. Thirty‐five‐day‐old male rats were subjected to 720° unilateral spermatic cord torsion of 9 hours duration. At the time of detorsion, animals were given a subcutaneous injection of i) cyclosporine, ii) prednisone, or iii) cyclosporine combined with prednisone. Control groups included: i) animals undergoing orchiectomy of the ipsilateral testis following the torsion period, ii) hemicastration in the absence of torsion and iii) sham surgery. Orchiectomy at the end of the torsion period prevented the torsion induced reduction of fertility, contralateral seminiferous tubule diameter and testis weight. Treatment with cyclosporine combined with prednisone significantly increased these parameters above detorsion alone. These data indicate that short term immunosuppression with cyclosporine alone or in combination with prednisone limits the adverse effects of unilateral spermatic cord torsion as does removal of the damaged organ at the end of the torsion period.
Unilateral spermatic cord torsion causes damage to the contralateral testis in humans and animal models. It is now known, however, at what age an animal's reproductive capacity is most susceptible to this type of trauma. To determine if the animal's age is a factor in its susceptibility to reproductive damage, rats at 30 to 70 days of age were subjected to unilateral spermatic cord torsion. Rats of the same ages underwent sham surgery and served as controls. The animals were allowed to recover from the surgery and to attain puberty before a period of fertility testing. Fertility, serum testosterone, organ weight, and testicular histologic data were obtained after the breeding period. Our data indicate that animals undergoing torsion at the youngest (30 days) and oldest (70 days) ages exhibited no change in the parameters studied. Animals between the ages of 35 and 50 days are highly susceptible to reproductive damage due to unilateral spermatic cord torsion, and the 35‐day‐old animals exhibit the most susceptibility. The stages of testicular development occurring during this period are such that damage to one testicle will result in degeneration of both organs. However, once the animal is older than 50 days, its reproductive capacity is not affected by spermatic cord torsion. The specific period of susceptibility in the development of human testes is yet to be defined.
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