Hyperdynamic sepsis depresses the circulatory compensation to
normovolemic anemia in conscious rats.
Morisaki, Hiroshi, William Sibbald, Claudio Martin, Gordon Doig, Kevin
Inman.
The A C Burton Vascular Biology Laboratory, Victoria Hospital
Research Institute, and The Program in Critical Care, University of
Western Ontario, London, Canada
APStracts 2:0418A, 1995.
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.
Using rat plasma, rat whole blood or packed rat RBCs, respectively,
randomization into three different hematocrit subgroups followed: low
(21-28%), middle (33-40%), and high (45-52%). Organ blood flows (Q)
were measured by the radioactive microsphere technique and organ
-QO2's were calculated. Twenty-four hours after laparotomy, the
hematocrit grouping had not modified the inter-organ distribution of
Q or QO2 in either the CLP or SHAM rats. To characterize overall
metabolic O2 reserve, rats were then exposed to hypoxia (FiO2 0.08)
for 20 minutes. While 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 CLP hematocrit subgroups. There was also a lesser
redistribution of QO2 away from the small intestine in the low
hematocrit CLP subgroup when compared to the high hematocrit
subgroup. We conclude that myocardial-QO2 is more effectively
maintained in septic hypoxic rats if the hematocrit is maintained at
levels greater than 45%.
Received 19 April 1995; accepted in final form 19 September 1995.
APS Manuscript Number A428-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95