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Department of Surgery, Program of Critical Care Medicine, Department of Pathology and Laboratory Medicine, and Pulmonary Research Laboratory, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6
We asked whether crystalloid administration improves tissue oxygen extraction in endotoxicosis. Four groups of anesthetized pigs (n = 8/group) received either normal saline infusion or no saline and either endotoxin or no endotoxin. We measured whole body (WB) and gut oxygen delivery and consumption during hemorrhage to determine the critical oxygen extraction ratio (ERO2 crit). Just after onset of ischemia (critical oxygen delivery rate), gut was removed for determination of area fraction of interstitial edema and capillary hematocrit. Radiolabeled microspheres were used to determine erythrocyte transit time for the gut. Endotoxin decreased WB ERO2 crit (0.82 ± 0.06 to 0.55 ± 0.08, P < 0.05) and gut ERO2 crit (0.77 ± 0.07 to 0.52 ± 0.06, P < 0.05). Unexpectedly, saline administration also decreased WB ERO2 crit (0.82 ± 0.06 to 0.62 ± 0.08, P < 0.05) and gut ERO2 crit (0.77 ± 0.07 to 0.67 ± 0.06, P < 0.05) in nonendotoxin pigs. Saline administration increased the area fraction of interstitial space (P < 0.05) and resulted in arterial hemodilution (P < 0.05) but not capillary hemodilution (P > 0.05). Saline increased the relative dispersion of erythrocyte transit times from 0.33 ± 0.08 to 0.72 ± 0.53 (P < 0.05). Thus saline administration impairs tissue oxygen extraction possibly by increasing interstitial edema or increasing heterogeneity of microvascular erythrocyte transit times.
oxygen delivery; oxygen consumption; endotoxemia; fluid administration; septic shock
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