Halothane prevents postischemic production of hydroxyl radicals in the canine heart

Lucio Glantz, Yehuda Ginosar, Mordechai Chevion, Yaacov Gozal, Amir Elami, Nahum Navot, Nahum Kitrossky, Benjamin Drenger

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32 Scopus citations


Background: Recent studies indicate that during regional myocardial ischemia and subsequent reperfusion, volatile anesthetics may provide protection against free radical-related injury. The effect of halothane on free radical production during ischemia and reperfusion, in the canine heart, was investigated. The level of hydroxyl radical (·OH)-mediated conversion of salicylate to its dehydroxybenzoate derivatives (2,3-DHBA and 2,5-DHBA) was monitored. Methods: Under general anesthesia, the heart was exposed through median sternotomy. Salicylate (100 mg/kg given intravenously) was administered 30 min before left anterior descending artery occlusion. Six dogs were studied using inhaled halothane (1.6%) 10 min before and during the 10-min ischethic period, followed by 50 min of reperfusion, and then they were compared with seven other dogs used as controls. Blood concentrations of salicylate, 2,3-DHBA and 2,5-DHBA, K+, lactate, oxygen content, and pH were monitored. Results: An acute increase in the normalized concentrations of 2,3-DHBA and 2,5-DHBA was observed in the control animals during reperfusion. In contrast, halothane inhalation completely inhibited the production of both metabolites (P< 0.02), but 2,5-DHBA concentrations in the halothane-treated group were even less than the basal level (P < 0.05). The increase in lactate concentrations in the experimental animals was significantly less than that of controls (P <0.05) and followed the same time-dependent pattern as the changes in K+ and pH. Halothane significantly decreased (P < 0.0001) the difference in oxygen content between coronary sinus and aortic root blood, suggesting decreased oxygen utilization during reperfusion. Conclusions: Halothane completely inhibited the production of ·OH, and its administration may protect the heart from the deleterious effect of oxygen-derived reactive species, with attenuation of the metabolic response to ischemia.

Original languageEnglish
Pages (from-to)440-447
Number of pages8
Issue number2
StatePublished - Mar 8 1997
Externally publishedYes


  • Anesthetics, volatile: halothane
  • Animal: dog
  • Dihydroxybenzoic acid
  • Electrochemical detection
  • Free radicals: hydroxyl radicals
  • Heart, coronary circulation: occlusion; regional ischemia
  • Heart, stunned myocardium: postischemic, reperfusion
  • Salicylate
  • high- pressure liquid chromatography

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    Glantz, L., Ginosar, Y., Chevion, M., Gozal, Y., Elami, A., Navot, N., Kitrossky, N., & Drenger, B. (1997). Halothane prevents postischemic production of hydroxyl radicals in the canine heart. Anesthesiology, 86(2), 440-447. https://doi.org/10.1097/00000542-199702000-00019