ALTERATION OF TESTICULAR MICROVASCULAR PRESSURES DURING VENOUS-PRESSURE ELEVATION

We have addressed the hypothesis that varicocele-related infertility i s caused in part by a pressure-induced disturbance of testicular conve ctive transport that upsets the testicular hormonal environment and th us impairs spermatogenesis. The left testis of the hamster [pentobarbi tal sodium (Nembutal), 70 mg/kg ip] was prepared for microcirculatory observations. Testicular venous pressure was acutely elevated by ligat ing collateral routes of venous outflow and partially occluding, via a snare, the main venous outflow distal to the pampiniform plexus. Simu ltaneous 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 postcapill ary venules. The data show that over 90% of the venous pressure elevat ion (VPE) was transmitted to the postcapillary venules. VPE affected i ntravascular pressures throughout the testis microvasculature; on aver age, capsular artery pressure increased by 83% of the VPE, although pa rt of this increase was due to a rise in systemic arterial pressure. V asoconstriction helped to buffer the pressure rise in the capsular art ery, probably at the expense of flow amplitude. Yet the vasoconstricti on was ineffective in preventing a rise in exchange vessel pressure. T hese data suggest that microvascular fluid exchange may be dramaticall y altered in varicocele, upsetting the hormonal and paracrine environm ent of the testis, and hence, impairing physiological regulation of ga metogenesis.