A Model of Brain Arteriolar Oxygen and Carbon Dioxide Transport during Anemia

Existing experimental and theoretical evidence suggests that precapillary diffusion of O 2 and CO 2 occurs between arterioles and tissue under normal physiologic conditions. However, limited information is available on arteriolar gas transport during anemia. With use of a mathematical model of an arteriolar network in brain tissue, anemic hematocrits of 35, 25, and 15% were modeled to determine the effect of anemia on the exchange, the change in the equilibrium tissue O 2 and CO 2 tensions, and the increase in blood flow needed to restore tissue oxygenation. We found that the blood Po 2 exiting the network fell from 66 mm Hg normally to 48 mm Hg during the severest anemia. Concurrently, the equilibrium tissue O 2 tensions dropped from 44 to 23 mm Hg. For CO 2 the exit blood Pco 2 was 58 mm Hg for a 15% hematocrit, an increase of 4 mm Hg from the normal value, and equilibrium tissue Pco 2 increased from 56 to 61 mm Hg. Blood flow increases from normal values necessary to offset the effects of the decreased O 2 delivery to the tissue were 26, 86, and 222%, respectively, for hematocrits of 35, 25, and 15%. We compared our model results with recent experimental studies that have suggested that the amount of O 2 diffusion is much higher than predicted values. We found that these experimental O 2 gradients are three to four times larger than theoretical.