Hyperdynamic sepsis depresses circulatory compensation to normovolemic anemia in conscious rats

Hiroshi Morisaki, William Sibbald, Claudio Martin, Gordon Doig, Kevin Inman

Research output: Contribution to journalArticlepeer-review

31 Citations (Scopus)


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%.

Original languageEnglish
Pages (from-to)656-664
Number of pages9
JournalJournal of Applied Physiology
Issue number2
Publication statusPublished - 1996 Feb
Externally publishedYes


  • hemodilution
  • hypoxia
  • oxygen delivery
  • regional blood flows
  • transfusion

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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