Desflurane-Induced Cardioprotection Against Ischemia-Reperfusion Injury Depends On Timing

• Published in: Journal of cardiothoracic and vascular anesthesia 2009-10, Vol.23 (5), p.600-606
• Main Authors: Smul, Thorsten M., MD, Lange, Markus, MD, Redel, Andreas, MD, Stumpner, Jan, MD, Lotz, Christopher A., MD, Roewer, Norbert, MD, PhD, Kehl, Franz, MD, PhD, DEAA
• Format: Article
• Language: English
• Subjects: Anesthesia & Perioperative Care; Animals; cardioprotection; Cardiotonic Agents - therapeutic use; Critical Care; desflurane; Ischemic Preconditioning, Myocardial - methods; Isoflurane - analogs & derivatives; Isoflurane - therapeutic use; Male; myocardial infarction; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - prevention & control; Neuroprotective Agents - therapeutic use; postconditioning; preconditioning; rabbit; Rabbits; reperfusion injury; Time Factors; volatile anesthetics
• ISSN: 1053-0770; 1532-8422
• DOI: 10.1053/j.jvca.2008.11.004

Objectives The authors tested the hypothesis that desflurane-induced cardioprotection depends on the timing of application and whether desflurane-induced postconditioning is mediated by nitric oxide. Design A prospective randomized vehicle-controlled study. Setting A university research laboratory. Subjects New Zealand White rabbits (N = 56). Interventions Rabbits 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. Results Infarct 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%). Conclusions Desflurane 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.