Alteration of testicular microvascular pressures during venous pressure elevation.

We have addressed the hypothesis that varicocele-related infertility is caused in part by a pressure-induced disturbance of testicular convective transport that upsets the testicular hormonal environment and thus impairs spermatogenesis. The left testis of the hamster [pentobarbital sodium (Nembutal), 70 mg/kg ip] was prepared for microcirculatory observations. Testicular venous pressure was acutely elevated by ligating collateral routes of venous outflow and partially occluding, via a snare, the main venous outflow distal to the pampiniform plexus. Simultaneous direct pressure measurements (servo-null method) were made to monitor venous pressure elevation and quantify resulting pressure and diameter changes in the arterial feed to the testis and in postcapillary venules. The data show that over 90% of the venous pressure elevation (VPE) was transmitted to the postcapillary venules. VPE affected intravascular pressures throughout the testis microvasculature; on average, capsular artery pressure increased by 83% of the VPE, although part of this increase was due to a rise in systemic arterial pressure. Vasoconstriction helped to buffer the pressure rise in the capsular artery, probably at the expense of flow amplitude. Yet the vasoconstriction was ineffective in preventing a rise in exchange vessel pressure. These data suggest that microvascular fluid exchange may be dramatically altered in varicocele, upsetting the hormonal and paracrine environment of the testis, and hence, impairing physiological regulation of gametogenesis.