In:
Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 13, No. 5 ( 1993-09), p. 872-880
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
0271-678X
,
1559-7016
DOI:
10.1038/jcbfm.1993.109
Language:
English
Publisher:
SAGE Publications
Publication Date:
1993
detail.hit.zdb_id:
2039456-1
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