Response of arterial resistance and critical pressure to changes in perfusion pressure in canine hindlimb

Abstract

The dynamic pressure-flow relationship in the canine hindlimb at normal arterial pressure is best explained by modeling a Starling resistor (critical pressure, Pcrit) at the level of the arterioles. Regulation of flow can therefore occur at the Starling resistor through changes in Pcrit or along the length of the vessel through changes in arterial resistance (Ra). We hypothesized that increasing perfusion pressure (Pper) would increase Pcrit due to the myogenic response but would decrease Ra because of flow-mediated vasodilation and passive effects. We pump-perfused vascularly isolated hindlimbs of anesthetized dogs and then measured Pcrit and calculated Ra over Pper range of 75-175 mmHg. When Pper was increased from 75 to 175 mmHg, Pcrit increased from 33 +/- 2 to 48 +/- 6 (means +/- SE) mmHg, whereas Ra decreased from 10.1 +/- 1.2 to 7.86 +/- 0.7 mmHg.min.100 g.ml-1 (P < 0.01). Thus the responses of Pcrit and Ra to an increase in Pper were dissociated. In a second part of the study, we lowered carotid sinus pressure to determine the effects of central factors on local autoregulation. A decrease in carotid sinus pressure increased Pcrit and Ra at each Pper (P < 0.05). We conclude that an increase in Pper causes the arterial vasculature to constrict at the level of the Starling resistor and dilate more proximally. The carotid baroreflex causes an increase in tone throughout the arterial vasculature but does not alter the local response to increases in Pper.