Effect of epinephrine on oxygen consumption and delivery during progressive hemorrhage.
Details
Serval ID
serval:BIB_25AB91C1A5F7
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Effect of epinephrine on oxygen consumption and delivery during progressive hemorrhage.
Journal
Critical Care Medicine
ISSN
0090-3493 (Print)
ISSN-L
0090-3493
Publication state
Published
Issued date
1995
Peer-reviewed
Oui
Volume
23
Number
7
Pages
1272-1278
Language
english
Notes
Publication types: Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Abstract
OBJECTIVE: To determine whether, during hemorrhagic shock, the effect of epinephrine on energy metabolism could be deleterious, by enhancing the oxygen requirement at a given level of oxygen delivery (DO2).
DESIGN: Prospective, randomized, control trial.
SETTING: Experimental laboratory.
SUBJECTS: Two groups of seven mongrel dogs were studied. The epinephrine group received a continuous infusion of epinephrine (1 microgram/min/kg) while the control group received saline.
INTERVENTION: Dogs were anesthetized with pentobarbital, and shock was produced by stepwise hemorrhage.
MEASUREMENTS AND MAIN RESULTS: Oxygen consumption (VO2) was continuously measured by the gas exchange technique, while DO2 was independently calculated from cardiac output (measured by thermodilution) and blood oxygen content. A dual-lines regression fit was applied to the DO2 vs. VO2 plot. The intersection of the two regression lines defined the critical value of DO2. Values above critical DO2 belonged to phase 1, while phase 2 occurred below critical DO2. In the control group, VO2 was independent of DO2 during phase 1; VO2 was dependent on DO2 during phase 2. In the epinephrine group, the expected increase in VO2 (+19%) and DO2 (+50%) occurred under normovolemic conditions. During hemorrhage, VO2 immediately decreased, and the slope of phase 1 was significantly (p < .01) different from zero, and was significantly (p < .05) steeper than in the control group (0.025 +/- 0.005 vs. 0.005 +/- 0.010). However, the critical DO2 (8.7 +/- 1.7 vs. 9.7 +/- 2.4 mL/min/kg), the critical VO2 (5.6 +/- 0.5 vs. 5.5 +/- 0.9 mL/min/kg), and the slope of phase 2 (0.487 +/- 0.080 vs. 0.441 +/- 0.130) were not different from control values.
CONCLUSIONS: The administration of pharmacologic doses of epinephrine significantly increased VO2 under normovolemic conditions due to the epinephrine-induced thermogenic effect. This effect progressively decreased during hemorrhage. The critical DO2 and the relationship between DO2 and VO2 in the supply-dependent phase of shock were unaffected by epinephrine infusion. These results suggest that during hemorrhagic shock, epinephrine administration did not exert a detrimental effect on the relationship between DO2 and VO2.
DESIGN: Prospective, randomized, control trial.
SETTING: Experimental laboratory.
SUBJECTS: Two groups of seven mongrel dogs were studied. The epinephrine group received a continuous infusion of epinephrine (1 microgram/min/kg) while the control group received saline.
INTERVENTION: Dogs were anesthetized with pentobarbital, and shock was produced by stepwise hemorrhage.
MEASUREMENTS AND MAIN RESULTS: Oxygen consumption (VO2) was continuously measured by the gas exchange technique, while DO2 was independently calculated from cardiac output (measured by thermodilution) and blood oxygen content. A dual-lines regression fit was applied to the DO2 vs. VO2 plot. The intersection of the two regression lines defined the critical value of DO2. Values above critical DO2 belonged to phase 1, while phase 2 occurred below critical DO2. In the control group, VO2 was independent of DO2 during phase 1; VO2 was dependent on DO2 during phase 2. In the epinephrine group, the expected increase in VO2 (+19%) and DO2 (+50%) occurred under normovolemic conditions. During hemorrhage, VO2 immediately decreased, and the slope of phase 1 was significantly (p < .01) different from zero, and was significantly (p < .05) steeper than in the control group (0.025 +/- 0.005 vs. 0.005 +/- 0.010). However, the critical DO2 (8.7 +/- 1.7 vs. 9.7 +/- 2.4 mL/min/kg), the critical VO2 (5.6 +/- 0.5 vs. 5.5 +/- 0.9 mL/min/kg), and the slope of phase 2 (0.487 +/- 0.080 vs. 0.441 +/- 0.130) were not different from control values.
CONCLUSIONS: The administration of pharmacologic doses of epinephrine significantly increased VO2 under normovolemic conditions due to the epinephrine-induced thermogenic effect. This effect progressively decreased during hemorrhage. The critical DO2 and the relationship between DO2 and VO2 in the supply-dependent phase of shock were unaffected by epinephrine infusion. These results suggest that during hemorrhagic shock, epinephrine administration did not exert a detrimental effect on the relationship between DO2 and VO2.
Keywords
Animals, Dogs, Drug Evaluation, Preclinical, Epinephrine/administration & dosage, Epinephrine/blood, Norepinephrine/blood, Oxygen Consumption/drug effects, Prospective Studies, Random Allocation, Shock, Hemorrhagic/drug therapy, Shock, Hemorrhagic/metabolism, Splenectomy, Statistics, Nonparametric
Pubmed
Web of science
Create date
05/03/2008 17:41
Last modification date
20/08/2019 14:04
Usage data
