MAXIMAL VASODILATION DOES NOT ELIMINATE THE VASCULAR WATERFALL IN THE CANINE HINDLIMB

Previous studies have shown that blood flow through skeletal muscle is regulated by changes in an arteriolar vascular waterfall [critical pressure (Pcrit)] and a proximal (arterial) resistance (Ra) element. To determine whether Pcrit still exists during maximal vasodilation, we pump perfused vascularly isolated canine hindlimbs. We set outflow pressure to zero and measured Pcrit, perfusion pressure (Pper), and regional elastic recoil pressure (Pel; by a stop-flow technique) and calculated both Ra and venous resistance before and after maximal vasodilation with adenosine and nitroprusside. Pcrit was 56.4 +/- 5.1 mmHg before vasodilation and 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 levels under vasodilated conditions. However, we could still measure Pcrit because our technique allowed Pel to decline and Pcrit becomes apparent once Pel < Pcrit. With vasodilation, Ra decreased to <8.1 +/- 2.6% and Rv decreased to 41 +/- 6% of control values. In contrast to the nonvasodilated vasculature, increases in venous pressure 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.