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Canadian Journal of Anesthesia

, Volume 46, Issue 11, pp 1076–1081 | Cite as

Beneficial effects of sevoflurane and desflurane against myocardial reperfusion injury after cardioplegic arrest

  • Benedikt Preckel
  • Volker Thämer
  • Wolfgang Schlack
Laboratory Investigations

Abstract

Purpose

To determine whether sevoflurane or desflurane offer additional protective effects against myocardial reperfusion injury after protecting the heart against the ischemic injury by cardioplegic arrest.

Methods

Isolated rat hearts in a Langendorff-preparation (n=9) were arrested by infusion of HTK cardioplegic solution and subjected to 30 min global ischemia followed by 60 min reperfusion (controls). An additional 18 hearts were subjected to the same protocol, and sevoflurane (n=9) or desflurane (n=9) was added to the perfusion medium during the first 30 min of reperfusion in a concentration corresponding to 1.5 MAC in rats. Left ventricular (LV) developed pressure and creatine kinase (CK) release were determined as indices of myocardial performance and cellular injury, respectively.

Results

The LV developed pressure recovered to 46 ± 7% of baseline in controls. Functional recovery during reperfusion was improved by inhalational anesthetics to 67 ± 3% (sevoflurane, P < 0.05) and 61 ± 5% of baseline (desflurane, P < 0.05), respectively. Peak CK release during early reperfusion was reduced from 52 ± 11 U·min−1·g−1 in controls to 34 ± 7 and 26 ± 7 U·min−1·g−1 in sevoflurane and desflurane treated hearts, respectively. The CK release during the first 30 min of reperfusion was reduced from 312 ± 41 U·g−1 in control hearts to 195 ± 40 and 206 ± 37 U·g−1 in sevoflurane and desflurane treated hearts.

Conclusion

After ischemic protection by cardioplegia, sevoflurane and desflurane given during the early reperfusion period offer additional protection against myocardial reperfusion injury.

Keywords

Creatine Kinase Halothane Sevoflurane Enflurane Desflurane 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

Objectif

Déterminer si le sévoflurane ou le desflurane offrent des effets protecteurs supplémentaires contre une lésion de reperfusion myocardique après qu’on a protégé le coeur contre l’ischémie par un arrêt cardioplégique.

Méthode

Des coeurs de rats isolés dans une préparation de Langendorff (n=9) ont été arrêtés par la perfusion d’une solution cardioplégique HTK et soumis pendant 30 min à une ischémie globale suivie de 60 min de reperfusion (témoins). D’autres coeurs (18) ont été soumis au même protocole, mais du sévoflurane (n=9) ou du desflurane (n=9) a été ajouté au liquide de perfusion pendant les 30 premières min de la reperfusion selon une concentration correspondant à 1,5 CAM chez les rats. La pression développée dans le ventricule gauche (VG) et la libération de créatine-kinase (CK) ont été déterminées en qualité d’indices de performance myocardique et de lésion cellulaire, respectivement.

Résultats

La pression du VG est revenue à 46 ± 7 % des valeurs de base dans les coeurs témoins. La récupération fonctionnelle pendant la reperfusion a été améliorée par les anesthésiques d’inhalation à 67 ± 3 % (sévoflurane, P < 0,05) et à 61 ± 5 % des données de base (desflurane, P < 0,05), respectivement. La libération maximale de CK au début de la reperfusion a été réduite de 52 ± 11 U·min−1·g−1, chez les témoins, à 34 ± 7 et à 26 ± 7 U·min−1·g−1 dans les coeurs traités avec le sévoflurane et le desflurane, respectivement. La libération de CK pendant les 30 premières min de la reperfusion a été réduite de 312 ± 41 U·g−1, chez les témoins, à 195 ± 40 et à 206 ± 37 U·g−1 dans les coeurs traités au sévoflurane et au desflurane.

Conclusion

Le sévoflurane et le desflurane administrés pendant le début d’une reperfusion, après qu’on a assuré une protection ischémique par cardioplégie, offrent une protection supplémentaire contre les lésions myocardiques de reperfusion.

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Copyright information

© Canadian Anesthesiologists 1999

Authors and Affiliations

  • Benedikt Preckel
  • Volker Thämer
    • 1
  • Wolfgang Schlack
  1. 1.Institut für Klinische Anaesthesiologie and Physiologisches Institut IHeinrich-Heine-UniversitätDüsseldorfGermany

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