Akademik Veri Yönetim Sistemi
Urology, cilt.51, sa.6, ss.1051-1056, 1998 (SCI-Expanded)
Objectives. The correlation between infertility and morphofunctional alterations following vasal occlusion is not clearly understood. Although a correlation has been found between the expression of a high titer of antisperm antibodies and the status of infertility, the relationship between the immunoglobulin (Ig) depositions in the testis and ultrastructural alterations of the peritubular structures has not been clearly established. The objective of this study is to explain the etiopathogenesis of diffuse and focal testicular lesions caused by vasal obstruction. Methods. Unilateral vasectomy was performed on adult male rats. Ultrastructural changes of testicular tissues and immunostaining affinity of peritubular structures with anti-actin, anti-vimentin, anti-laminin, and anti-immunoglobulin G (anti- IgG) antibodies were analyzed. Results. In an ultrastructural study, vasectomized animals presented abundant collagen fibril accumulation in the peritubular area. In testis with intense IgG antibodies, staining revealed weak immunostaining of peritubular myoid cells with anti-actin antibodies, but intense immunostaining with anti-vimentin antibodies. The tubules of rats with no IgG deposition on peritubular structures revealed intense immunostaining with anti-actin antibodies but scant immunostaining with anti- vimentin antibodies. Anti-laminin deposits decreased severely in most of the tubules demonstrating intense IgG deposition. Conclusions. Our findings suggest that spermatogenesis deteriorates more severely in testes with dense IgG deposition. The sclerosis of the lamina propria in cases with vasal occlusion is secondary to alterations in the peritubular myoid cells. With the progressive changes that occur in the peritubular myoid cells or differentiation of the peritubular myoid cells that acquire active cell characteristics, collagen accumulation adjacent to these cells increases markedly. The alterations of the peritubular myoid cells reported here may be caused by alterations in basement membrane structures.