Effect of hematocrit on systemic O2 transport in hypoxic and normoxic exercise in rats.
The effect of hematocrit (Hct) on O2 transport in hypoxic [inspired PO2 (PIO2) approximately 70 Torr] and normoxic (PIO2 approximately 145 Torr) exercise was studied in rats acclimatized to 3 wk of PIO2 at approximately 70 Torr (A rats) and in nonacclimatized littermates (NA rats). Isovolumic exchange transfusion of plasma or red blood cells was used to lower Hct in A rats from approximately 60 to 45% and to raise Hct of NA rats from 45 to 60%: Controls were A and NA rats exchange transfused with whole blood at constant Hct. Lowering Hct of A rats lowered the arterial O2 concentration (CaO2) and the arterial-mixed venous O2 difference and increased the maximal cardiac output (Qmax) without changes in maximal O2 uptake (VO2 max) or in the product of Qmax x CaO2, circulatory O2 convection at maximal exercise (TO2 max). Raising Hct in NA rats produced the opposite changes in CaO2, arterial-mixed venous O2 difference, and Qmax, but VO2 max and TO2 max increased significantly, both in hypoxia and normoxia, because of relatively small changes in Qmax. In NA rats, a steeper slope of the line relating VO2 max to calculated mean capillary PO2 at high Hct suggested a higher tissue O2 diffusing capacity with high Hct. For a given Hct and Qmax, systemic arterial pressure was higher in A rats. The data suggest that 1) the effect of Hct on systemic hemodynamics is different in A and NA rats, resulting in different effects on VO2 max; 2) factors in addition to Hct contribute to the high systemic vascular resistance of A rats; and 3) increased diffusive conductance for O2, as well as increased TO2 max, could be responsible for the effect of Hct on VO2 max of NA rats.[1]References
- Effect of hematocrit on systemic O2 transport in hypoxic and normoxic exercise in rats. Gonzalez, N.C., Erwig, L.P., Painter, C.F., Clancy, R.L., Wagner, P.D. J. Appl. Physiol. (1994) [Pubmed]
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