Maximal vasodilation does not eliminate the vascular waterfall in the canine hindlimb. Shrier, I., and S. Magder. Dr. I. Shrier, Herzl Family Practice Centre Rm. E-0010, Sir Mortimer B. Davis Jewish General Hospital, 5757 Legare, Montreal, Qc. H3T 1Z6, (Tel) 514-340-8253, (FAX) 514-842-6866
APStracts 2:0262A, 1995.
Previous studies have shown that blood flow through skeletal muscle is regulated by changes in an arteriolar vascular waterfall (Pcrit ) and a proximal resistance element (Rart). To determine if Pcrit still exists during maximal vasodilation, we pump-perfused vascularly isolated canine hindlimbs. We set outflow pressure (Pven) to zero and measured Pcrit, perfusion pressure (Pper), the regional elastic recoil pressure (Pel, by a stop-flow technique), and calculated both Rart and venous resistance (Rven) before and after maximal vasodilation with adenosine and nitroprusside. Pcrit was 56.4+/-5.1 mmHg before vasodilation. Pcrit decreased to 11.0+/-0.6 mmHg after vasodilation which was less than the downstream pressure in the venous compliant region (Pel). Therefore Pcrit should not have affected flow at normal Pper under vasodilated conditions. However, we could still measure Pcrit because our technique allowed Pel to decline, and Pcrit becomes apparent once Pel&LTPcrit. With vasodilation, Rart decreased to less than 8.1+/-2.6% and Rven to 41+/-6% of control. In contrast to the non-vasodilated vasculature, increases in Pven during maximal vasodilation caused immediate increases in Pper. This also suggests that the vascular waterfall is inactive under conditions of maximal vasodilation. We conclude that a small arteriolar Pcrit is still present in the maximally vasodilated hindlimb but is less than the downstream pressure, and does not affect flow under these conditions.

Received 20 December 1994; accepted in final form 5 June 1995.
APS Manuscript Number A1290-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  6 July 1995.