Journal of Applied Physiology, Vol 51, Issue 3 565-570, Copyright © 1981 by American Physiological Society
Blood flow and O2 uptake in dog hindlimb with anemia, norepinephrine, and propranolol
C. K. Chapler and S. M. Cain
To examine the relative importance of 1) reduced blood viscosity, 2)
vasodilation mediated through beta-adrenergic receptors, and 3) sympathetic
nerve activity on the regulation of limb blood flow during anemia,
norepinephrine (NE) was infused in 10 anesthetized-paralyzed dogs at normal
and reduced hematocrit (Hct). Cardiac output (QT), limb and total oxygen
uptake (VO2)n and limb venous flow (QL) were determined. After a control
period, NE (2 micrograms . kg-1 . min-1) was infused followed by another
control period. The Hct was then reduced to 9% by isovolemic hemodilution
with dextran, and data were obtained during anemia, anemia plus NE, and
after isovolemic reinfusion of red blood cells (Hct 25%) during NE. Another
10 dogs were treated identically after propranolol (1.0 mg/kg)
administration. At normal Hct, NE increased limb resistance (RL) (P less
than 0.01) in the beta-block group; a decrease in RL (P less than 0.05) and
a rise in QL (P less than 0.01) occurred in the no block group. QL and VO2
(limb and total) were not changed by NE. During anemia, RL was not altered
in either group by NE; QT fell (P less than 0.05) in both, and QL decreased
in the no block group. After reinfusion of cells, NE produced an increase
in RL and total peripheral resistance (P less than 0.01) and a fall in QL
(P less than 0.01) and QT (P less than 0.01) in both groups; limb and total
VO2 rose in the no block group. We conclude that the reduction in viscosity
prevented an increase in both RL and redistribution of QL during severe
anemia (Hct 9%).
