@entity842 produced in the testis is involved in dilatation of the internal spermatic vein that compromises spermatogenesis in infertile XXXX with varicocele.

@entity3623 @entity1 @entity842 @entity1110
OBJECTIVE: To determine the concentration of @entity842 (NO) and the location and change in the expression of @entity3623 ( @entity3623 ) isoforms in the testes of subfertile @entity1 with varicocele, and to compare the NO concentration or @entity3623 expression with clinical variables, to determine the role of NO on the pathophysiology of varicocele. @entity1 AND METHODS: In all, 27 @entity1 who had a left varicocelectomy and five with 'normal' spermatogenesis (controls) who had scrotal surgery for other reasons were enrolled. Intratesticular fluid was taken from the @entity1 and the NO concentration determined colorimetrically. The expression and location of @entity3623 isoforms were examined by Western blotting and immunohistochemistry, using testicular biopsy specimens, and @entity1110 -diaphorase ( @entity1110 -d) staining used to identify NO-producing cells. The relationship between the NO concentration and the expression of @entity3623 isoforms or clinicopathological variables was investigated. RESULTS: In testes with grade 2 and 3 varicoceles there were significant increases in the concentration of NO or the expression of inducible @entity3623 . There was no change in the expressions of endothelial @entity3623 , which is located in vascular endothelial cells, while @entity1110 -d activity was mainly located in these cells. The concentration of NO was significantly correlated with the maximum and total vein diameter (both P<0.01). In @entity1 aged>35 years, the concentration of NO significantly correlated with a deterioration in total motile sperm count (P<0.05). CONCLUSIONS: Increased production of NO in the testis is involved in the enlargement of varicocele and indirectly deteriorates spermatogenesis.
