Abstract

The mechanism of deterioration of ipsilateral and contralateral testes during unilateral maldescent remains controversial. Proposing that alterations in tissue perfusion may play a role in ipsilateral and contralateral testicular deteriorations, an experimental study has been planned to evaluate the status of parameters of tissue hypoxia in ipsilateral and contralateral testes following surgically induced maldescent, in rats which preoperatively underwent placebo or chemical sympathectomy. 60 male albino rats were used for the experiment. At the age of 21 days each 30 rats that were treated by placebo or chemical sympathectomy agent were divided into 3 groups undergoing sham operation, abdominal fixation of one testis or abdominal fixation of both testes. At the age of 3 months the rats underwent bilateral orchidectomies and lactic acid (LA) and hypoxanthine (HX) levels were measured in testicular tissues. Maldescent of the testis resulted in a marked increase of LA and HX values in the ipsilateral testis compared to controls, and also resulted in increased levels of LA and HX in the contralateral testis. Although the levels of LA and HX were lower compared to ipsilateral undescended counterparts the levels in contralateral testis were significantly elevated compared to the contralateral testes of rats undergoing sham operation following placebo treatment. Bilateral maldescent resulted in similar elevations of LA and HX in both of the testes. Administration of 6-hydroxydopamine did not result in decreased levels of LA and HX values in the ipsilateral testis following unilateral testicular undescendence. However the LA levels in the contralateral descended testis did not reveal a significant difference compared to the contralateral testis of rats undergoing sham operation. The present experimental design reveals that abdominal fixation of the testis results in tissue hypoxia not only in the ipsilateral but also in the contralateral testis. Chemical sympathectomy has some protective effects on contralateral testicular hypoxia during unilateral maldescent. Tissue hypoxia during maldescent may result from relative inadequacy of testicular blood flow to overcome the increased metabolic demands under hyperthermic conditions.

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