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Hydroxyl radical formation during inhalation anesthesia in the reperfused working rat heart



To determine whether isoflurane, sevoflurane and halothane influenced hydroxyl radical production in the ischemic rat heart.


Twenty-four male Wistar rats were divided into four groups; control (C), isoflurane 1.4% (I), sevoflurane 2.5% (S) and halothane 1% (H). The hearts were perfused with modified Krebs-Henseleit bicarbonate buffer by a working heart model for 10 min. Then, whole heart ischemia was induced by severely restricting coronary perfusion for 15 min. Reperfusion of the hearts after this ischemic period lasted for 20 min. The coronary effluent was collected before and during ischemia and at 1,5,10,20 min after reperfusion. At the end of reperfusion, hearts were removed and prepared for measurement. Hydroxyl radicals were identified by their reaction with salicylic acid to yield dihydroxybenzoic acids (DHBAs).


Before and after ischemia, there were no differences in coronary flow and heart rate among the four groups, but cardiac output and LV dP/dt maximum in the anesthetic groups were lower than in the control group. Hydroxyl radical products in the heart were significantly lower in the I group than the other groups (e.g. C vs I, 278.1 ± 24.3 vs 219.3 ± 14.4 μM· g−1,P < 0.05). The concentrations of DHBAs in the coronary effluent at some points in the I and H groups were less than in the C and S groups.


These results indicate that isoflurane and halothane (to a lesser extent), reduce hydroxyl radical production in the ischémie heart, but sevoflurane does not.



Déterminer si l’isoflurane, le sevoflurane et l’halothane ont influencé la production de radical hydroxyle dans des coeurs de rats ischémiques.


Vingt-quatre rats mâles Wistar ont été répartis en quatre groupes: témoin (T), isoflurane 1,4 % (I), sevoflurane 2,5 % (S) et halothane I% (H). Les coeurs ont été perfuses avec une solution tampon modifiée de bicarbonate Krebs-Henseleit selon un modèle de travail cardiaque pendant 10 min. Ensuite, une ischémie cardiaque totale a été induite en limitant la perfusion coronaire de façon importante pendant 15 min. À la suite de quoi, la reperfusion a duré 20 min. Leffluent coronarien a été recueilli avant et pendant l’ischémie et à 1,5,10,20 min après la reperfusion. À la fin de la reperfusion, les coeurs ont été retirés et préparés pour l’étude. Les radicaux hydroxyles ont été identifiés par leur réaction avec l’acide salicylique pour produire des acides dihydroxybenzoïques (ADHB).


Avant et après l’ischémie, il n’y avait pas de différence de flux coronarien et de fréquence cardiaque intergroupe, mais le débit cardiaque et le dp/dt maximal du VG dans les groupes I, S et H étaient plus faibles que dans le groupe T. La production de radical hydroxyle dans le coeur était moins importante dans le groupe I que dans les autres groupes (par ex. C vs I, 278,1 ± 24,3 vs 219,3 ± 14,4 μM·g−1,P < 0,05). Les concentrations d’ADHB de l’effluent dans les groupes I et H ont été, à quelques reprises, plus faibles que dans les groupes C et S.


L’isoflurane et l’halothane (à un moindre degré) réduisent la production de radical hydroxyle dans le coeur ischémique, contrairement au sévoflurane.


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Correspondence to Satoshi Kashimoto.

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Nakamura, T., Kashimoto, S., Oguchi, T. et al. Hydroxyl radical formation during inhalation anesthesia in the reperfused working rat heart. Can J Anesth 46, 470 (1999).

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  • Isoflurane
  • Halothane
  • Sevoflurane
  • Coronary Flow
  • Inhalation Anesthetic