Response of arterial resistance and critical pressure to changes in perfusion pressure in canine hindlimb
Shrier, I.; Magder, S.
American Journal of Physiology 265(6 Pt 2): H1939-H1945
1993
ISSN/ISBN: 0002-9513 PMID: 8285232 Document Number: 409591
The dynamic pressure-flow relationship in the canine hindlimb at normal arterial pressure is best explained by modeling a Starling resistor (critical pressure, P-crit) at the level of the arterioles. Regulation of flow can therefore occur at the Starling resistor through changes in P-crit or along the length of the vessel through changes in arterial resistance (R-a). We hypothesized that increasing perfusion pressure (P-per) would increase P-crit due to the myogenic response but would decrease R-a because of flow-mediated vasodilation and passive effects. We pump-perfused vascularly isolated hindlimbs of anesthetized dogs and then measured P-crit and calculated R-a over P-per range of 75-175 mmHg. When P-per was increased from 75 to 175 mmHg, P-crit increased from 33 +- 2 to 48 6 (means SE) mmHg, whereas R-a decreased from 10.1 +- 1.2 to 7.86 +- 0.7 mm.Hg cntdot min cntdot 100 g cntdot ml-1 (P lt 0.01). Thus the responses of P-crit and R-a to an increase in P-per 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 P-crit and R-a at each P-per (P lt 0.05). We conclude that an increase in P-per 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 P-per.