Hyperdynamic sepsis depresses circulatory compensation to normovolemic anemia in conscious rats

This study was designed to determine whether sepsis modifies the ability to preserve vital organ O₂ delivery (Q̇O₂) 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 (4552%). Organ blood flow values (Q̇) were measured by the radioactive microsphere technique, and organ Q̇O₂ values were calculated. Twenty-four hours after laparotomy, the hematocrit grouping had not modified the interorgan distribution of Q̇ or Q̇O₂ 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 Q̇O₂ 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 Q̇O₂ away from the small intestine in the low-hematocrit compared with the high-hematocrit CLP subgroup. We conclude that myocardial Q̇O₂ is more effectively maintained in septic hypoxic rats if the hematocrit is maintained at levels >45%.