British Journal of Anaesthesia, 2002, Vol. 88, No. 4 546-554
© 2002 The Board of Management and Trustees of the British Journal of Anaesthesia
Laboratory Investigations |
Xenon increases total body oxygen consumption during isoflurane anaesthesia in dogs
Departments of 1Anaesthesiology and 2Physiology, Heinrich-Heine-University, Moorenstrasse 5, D-40225 Düsseldorf, Germany*Corresponding author
Background. This study was designed to examine whether the coupling between oxygen consumption (V·O2) and cardiac output (CO) is maintained during xenon anaesthesia.
Methods. We studied the relationship between V·O2 (indirect calorimetry) and CO (ultrasound flowmetry) by adding xenon to isoflurane anaesthesia in five chronically instrumented dogs. Different mixtures of xenon (70% and 50%) and isoflurane (0–1.4%) were compared with isoflurane alone (1.4% and 2.8%). In addition, the autonomic nervous system was blocked (using hexamethonium) to study its influence on V·O2 and CO during xenon anaesthesia.
Results. Mean (SEM) V·O2 increased from 3.4 (0.1) ml kg–1 min–1 during 1.4% isoflurane to 3.7 (0.2) and 4.0 (0.1) ml kg–1 min–1 after addition of 70% and 50% xenon, respectively (P<0.05), whereas CO and arterial pressure remained essentially unchanged. In contrast, 2.8% isoflurane reduced both, V·O2 [from 3.4 (0.1) to 3.1 (0.1) ml kg–1 min–1] and CO [from 96 (5) to 70 (3) ml kg–1 min–1] (P<0.05). V·O2 and CO correlated closely during isoflurane anaesthesia alone and also in the presence of xenon (r2=0.94 and 0.97, respectively), but the regression lines relating CO to V·O2 differed significantly between conditions, with the line in the presence of xenon showing a 0.3–0.6 ml kg–1 min–1 greater V·O2 for any given CO. Following ganglionic blockade, 50% and 70% xenon elicited a similar increase in V·O2, while CO and blood pressure were unchanged.
Conclusions. Metabolic regulation of blood flow is maintained during xenon anaesthesia, but cardiovascular stability is accompanied by increased V·O2. The increase in V·O2 is independent of the autonomic nervous system and is probably caused by direct stimulation of the cellular metabolic rate.
Br J Anaesth 2002; 88: 546–54
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