Abstract
Purpose
To investigate the effects of halothane and halothane plus vitamin E treatment on myocardial free radical metabolism in guinea pigs.
Methods
Four groups of seven animals were studied; control, halothane, halothane plus vitamin E and vitamin E groups. In the halothane group, halothane 1.5% in oxygen was given for 90 min over three days. In the halothane plus vitamin E group, 300 rng · kg−1 · day−1 vitamin Eim was started three days before the first halothane treatment and continued for three days. Following sacrifice, the hearts were assayed for superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) and malondialdehyde (MDA) level was determined. Electron spin resonance (ESR) analysis and electron microscopy (EM) were also performed.
Results
In the halothane group, SOD activities and MDA concentrations were increased compared with control and GSH-Px and CAT activities were decreased. In the halothane plus vitamin E group, there were no differences in enzyme activity compared with halothane alone but the MDA level was decreased. In the vitamin E group, enzyme activities were increased compared with control. Mainly the CF3CHCl radical was identified by ESR analysis in heart tissues exposed to halothane and the concentration of this radical was reduced by vitamin E. Electron microscopy showed cytoplasmic vacuolisation and dilation in sarcoplasmic reticulum in the heart tissues exposed to halothane: both were prevented by vitamin E.
Conclusion
Although halothane causes impairment in enzymatic antioxidant defence potential, due to lowered GSH-Px and CAT activity, and accelerates peroxidative reactions in the tissues affected, no subcellular damage occurred. Vitamin E may protect tissues against free radical attack by scavenging toxic free radicals formed in heart tissue during halothane anaesthesia.
Résumé
Objectif
Étudier les effets de l’halothane et de l’association halothane-vitamine E sur la production myocardique de radicaux libres.
Méthodes
L’étude portait sur quatre groupes de sept animaux: contrôle, halothane, halothane+vitamine E, et vitamine E. Le groupe halothane a reçu de l’halothane 1,5% en oxygène pendant 90 min pour 3 jours. Le groupe halothane+vitamine E a reçu une doseim de 300 mg · kg−1 · j−1 de vitamine E pendant trois jours avant un premier traitement a l’halothane. Une fois l’animal sacrifié, la superoxyde dismutase (SOD), la glutathion peroxydase (GSH-Px) et catalase (CAT), et la malondialdéhyde (MDA) ont été titrées dans le tissu cardiaque. La résonance paramagnétique électronique (RPÉ) et la microscopie électronique ont complété ces analyses.
Résultats
Dans le groupe halothane, l’activité de la SOD et la concentration de MDA augmentaient comparativement au contrôle et l’activité de la GSH-Px et de la CAT diminuait. Dans le groupe halothane+vitamine E, l’activité enzymatique ne changeait pas comparativement à l’halothane seul mais le niveau de MDA diminuait. Dans le groupe vitamine E, l’activité enzymatique augmentait comparativement au contrôle. Le radical CF3CHCl était principalement identifié par l’analyse RPÉ dans le tissu cardiaque exposé à l’halothane alors que la vitamine E diminuait la concentration de ce radical. La microscopie électronique révélait une vacuolisation et une dilatation cytoplasmiques du réticulum sarcoplasmique du tissu cardiaque exposé à l’halothane; la vitamine E prévenait ces effets.
Conclusion
Malgré l’altération par l’halothane de la capacité de protection enzymatique contre l’oxydation, due à la baisse de l’activité de la GSH-Px et de la CAT et l’accélération des réactions peroxydatives dans les tissus affectés, il n’y a pas eu de dommages infracellulaires. La vitamine E protège les tissus contre l’agression des radicaux libres en épurant les radicaux toxiques libérés dans le tissu cardiaque pendant l’anesthésie à l’halothane.
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Durak, I., Kurtipek, O., Öztürk, H.S. et al. Impaired antioxidant defence in guinea pig heart tissues treated with halothane. Can J Anaesth 44, 1014–1020 (1997). https://doi.org/10.1007/BF03011975
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DOI: https://doi.org/10.1007/BF03011975