• Thorsten M Smul, Markus Lange, Andreas Redel, Jan Stumpner, Christopher A Lotz, Norbert Roewer, and Franz Kehl.
• Department of Anesthesiology, University of Würzburg, Würzburg, Germany.
• J. Cardiothorac. Vasc. Anesth. 2009 Oct 1; 23 (5): 600-6.

ObjectivesThe authors tested the hypothesis that desflurane-induced cardioprotection depends on the timing of application and whether desflurane-induced postconditioning is mediated by nitric oxide.DesignA prospective randomized vehicle-controlled study.SettingA university research laboratory.SubjectsNew Zealand White rabbits (N = 56).InterventionsRabbits were instrumented and subjected to a 30-minute coronary artery occlusion (CAO) and 3 hours of reperfusion. Animals were randomized to 8 groups (n = 7) and received 0.0 or 1.0 minimum alveolar concentration desflurane for 30 minutes before CAO (PRE), during CAO (ISCH), after CAO (POST), before and after CAO (PRE + POST), or continuously for 90 minutes starting 30 minutes before CAO (PRE + ISCH + POST). In 2 separate experimental groups, the nitric oxide synthase inhibitor N-omega-nitro-L-arginine (L-NA) was administered before reperfusion in the presence or absence of desflurane. Data are mean +/- standard deviation.ResultsInfarct size was 68% +/- 14% in control experiments. Desflurane significantly (p < 0.05) reduced infarct size in the PRE (43% +/- 9%) and POST groups (49% +/- 12%) but not in the ISCH group (69% +/- 9%). The PRE + ISCH + POST and PRE + POST groups produced similar reductions in infarct size to 47% +/- 12% and 43% +/- 9%, respectively. L-NA alone had no effect on infarct size (61% +/- 9%) but blocked postconditioning completely (L-NA + POST, 68% +/- 10%).ConclusionsDesflurane induces pre- and postconditioning but does not confer cardioprotection during ischemia in rabbits. The combination of pre- and postconditioning or continuous application does not provide additional cardioprotection. Furthermore, desflurane-induced postconditioning is mediated by nitric oxide.

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