Journal of Applied Physiology, Vol 65, Issue 5 2069-2074, Copyright © 1988 by American Physiological Society
Regional hemodynamic responses to hypoxia in polycythemic dogs
R. L. Stork, D. L. Bredle, C. K. Chapler and S. M. Cain
Department of Physiology and Biophysics, University of Alabama, Birmingham 35294.
Polycythemia increases blood viscosity so that systemic O2 delivery (QO2)
decreases and its regional distribution changes. We examined whether
hypoxia, by promoting local vasodilation, further modified these effects in
resting skeletal muscle and gut in anesthetized dogs after hematocrit had
been raised to 65%. One group (CON, n = 7) served as normoxic controls
while another (HH, n = 6) was ventilated with 9% O2--91% N2 for 30 min
between periods of normoxia. Polycythemia decreased cardiac output so that
QO2 to both regions decreased approximately 50% in both groups. In
compensation, O2 extraction fraction increased to 65% in muscle and to 50%
in gut. When QO2 was reduced further during hypoxia, blood flow increased
in muscle but not in gut. Unlike previously published normocythemic
studies, there was no initial hypoxic vasoconstriction in muscle. Metabolic
vasodilation during hypoxia was enhanced in muscle when blood O2 reserves
were first lowered by increased extraction with polycythemia alone. The
increase in resting muscle blood flow during hypoxia with no change in
cardiac output may have decreased O2 availability to other more vital
tissues. In that sense and under these experimental conditions,
polycythemia caused a maladaptive response during hypoxic hypoxia.
