Alteration of testicular microvascular pressures during venous
pressure elevation.
Sweeney, Terrence E., John S. Rozum, and Robert W. Gore.
Department of Biology, University of Scranton, Scranton, PA, 18509
and Department of Physiology, University of Arizona College of
Medicine, Tucson, AZ 85724
APStracts 2:0016H, 1995.
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
(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 post-capillary
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.
Received 13 October 1994; accepted in final form 24 January 1995.
APS Manuscript Number H919-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 February 1995.