Varicocele, a lesion primarily of the left spermatic vein, occurs only in human males and is associated with male infertility. Little is known about the cause-effect relationship between unilateral varicocele and its bilateral impairment of testis function. Still, a standard surgical treatment exists for this human lesion, again with no real understanding of how (or even if) the surgical intervention actually returns testis physiology to normal. This lack of knowledge is primarily due to the historical lack of experimental models of the lesion. Previous work from this and other laboratories has shown that experimental varicocele can be induced in several species by partial obstruction of the left renal vein. This unilateral experimental varicocele causes a bilateral increase in both testicular blood flow and temperature. Increases in testicular temperature are known to impair spermatogenesis. The present application proposes to investigate the mechanism behind the changes in blood flow and temperature. We will determine whether the bilateral response to the unilateral lesion is due to neural or vascular mediation and whether the ipsilateral testis, adrenal, or kidney is involved in the response of the contralateral testis to the unilateral experimental varicocele. Using radiolabelled microsphere distribution techniques, in vivo micropuncture, and analytical microtechniques we will determine testicular blood flow and temperature, testicular arterial and venous PO2, PCO2, pH, glucose concentrations testosterone concentrations, and cauda epididymidal sperm motility and concentration in normal animals. We will also make these determinations in animals with varicocele, repaired varicoceles, and varicocele + several treatments imposed to help determine the mechanism behind the antifertility effects of varicocele. This work will provide unique information on the effects of experimental varicocele and is important to the further understanding of human varicocele.
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