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 O-2 delivery (Q over dot O-2) 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 over dot) were measured by the radioactive microsphere technique, and organ Q over dot O-2 values were calculated. Twenty-four hours after laparotomy, the hematocrit grouping had not modified the interorgan distribution of Q over dot or Q over dot O-2 in either the CLP or Sham rats. To characterize overall metabolic O-2 reserve, rats were then exposed to hypoxia (inspired O-2 fraction, 0.08) for 20 min. Whereas cardiac output increased significantly during hypoxia in all experimental groups, myocardial Q over dot O-2 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 Q over dot O-2 away from the small intestine in the low-hematocrit compared with the high-hematocrit CLP subgroup. We conclude that myocardial Q over dot O-2 is more effectively maintained in septic hypoxic rats if the hematocrit is maintained at levels >45%.