Journal of Applied Physiology, Vol 80, Issue 2 656-664, Copyright © 1996 by American Physiological Society

ARTICLES

Hyperdynamic sepsis depresses circulatory compensation to normovolemic anemia in conscious rats

H. Morisaki, W. Sibbald, C. Martin, G. Doig and K. Inman
The A. C. Burton Vascular Biology Laboratory, Victoria Hospital Research Institute, University of Western Ontario, London, Canada.

This study was designed to determine whether sepsis modifies the ability to preserve vital organ O2 delivery (QO2) across a clinically relevant range of hematocrits. Ninety rats were randomly allocated to cecal ligation and perforation (CLP) or a sham (Sham) procedure. With the use of rat plasma, rat whole blood, or packed rat red blood cells, respectively, randomization into three different hematocrit subgroups followed: low (21-28%), middle (33-40%), and high (45-52%). Organ blood flow values (Q) were measured by the radioactive microsphere technique, and organ QO2 values were calculated. Twenty-four hours after laparotomy, the hematocrit grouping had not modified the interorgan distribution of Q or QO2 in either the CLP or Sham rats. To characterize overall metabolic O2 reserve, rats were then exposed to hypoxia (inspired O2 fraction, 0.08) for 20 min. Whereas cardiac output increased significantly during hypoxia in all experimental groups, myocardial QO2 failed to increase in the low hematocrit Sham subgroup and fell significantly in both the middle- and low-hematocrit CLP subgroups. There was also a lesser redistribution of QO2 away from the small intestine in the low-hematocrit compared with the high-hematocrit CLP subgroup. We conclude that myocardial QO2 is more effectively maintained in septic hypoxic rats if the hematocrit is maintained at levels >45%.

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