The variations in oxygen tension in relation to induced changes in the hematocrit, were investigated in mouse pneumoperitoneum and rat skin pockets.

A close to linear relationship was found in the range of hematocrit from 20-60 percent. Above this hematocrit value, the correlation was lost and no further increase in Po2 was noted with increases in the hematocrit. A tendency to a minor fall in Po2 at very high hematocrit values was observed in both systems, however, the fall was never below normal value.

Attempts to induce normovolemic erythrocytosis by exchange transfusions in rat demonstrated that this condition is transient, transforming into a hypervolemic erythrocytosis within hours. In spite of the increasing viscosity of the blood with increases in hematocrit, a hypervolemic erythrocytosis was found to cause a slight increase in tissue Po2 while a normovolemic erythrocytosis did not. Consequently, an accelerated rate of red cell production will have a dual effect on oxygen transport: (1) it will increase the oxygen carrying capacity, and (2) it will increase the blood volume and thereby decrease the peripheral resistance, allowing the heart to transport more oxygen at no extra expense.

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