Propofol Inhibits Desflurane-Induced Preconditioning in Rabbits

• Published in: Journal of cardiothoracic and vascular anesthesia Vol. 25; no. 2; pp. 276 - 281
• Main Authors: Smul, Thorsten M., Stumpner, Jan, Blomeyer, Christoph, Lotz, Christopher, Redel, Andreas, Lange, Markus, Roewer, Norbert, Kehl, Franz
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.04.2011
• Subjects: Anesthesia & Perioperative Care; Animals; cardioprotection; Critical Care; desflurane; Ischemic Preconditioning, Myocardial - methods; Isoflurane - analogs & derivatives; Isoflurane - antagonists & inhibitors; Isoflurane - pharmacology; Isoflurane - therapeutic use; Male; myocardial infarction; Myocardial Infarction - drug therapy; Myocardial Infarction - pathology; preconditioning; propofol; Propofol - pharmacology; Prospective Studies; rabbit; Rabbits; Random Allocation; reactive oxygen species; volatile anesthetics; propofol; desflurane; myocardial infarction; rabbit; reactive oxygen species; cardioprotection; volatile anesthetics; preconditioning
• ISSN: 1053-0770; 1532-8422; 1532-8422
• DOI: 10.1053/j.jvca.2010.07.018

The authors tested the hypothesis that ischemic and desflurane-induced preconditioning are blocked by propofol. A prospective, randomized, vehicle-controlled study. A university research laboratory. New Zealand white rabbits (n = 52). Pentobarbital-anesthetized rabbits were subjected to 30 minutes of coronary artery occlusion followed by 3 hours of reperfusion. Rabbits received 0.0 (control) or 1.0 minimum alveolar concentration of desflurane (30 minutes‘ duration and a 30-minute memory period) or ischemic preconditioning (5 minutes of ischemia and a 30-minute memory period) in the absence or presence of propofol (10 mg/kg/h intravenously) or its vehicle (10% Intralipid emulsion; B Braun, Melsungen, Germany). The myocardial infarct size was measured with triphenyltetrazolium staining. Statistical analysis was performed with 1-way and 2-way analysis of variance when appropriate, followed by a post hoc Duncan test. Data are mean ± standard deviation. Myocardial infarct size was 56% ± 8% in control animals (n = 7). Desflurane significantly ( p < 0.05) reduced the infarct size to 37% ± 6% (n = 7). Desflurane-induced preconditioning was blocked by propofol (65% ± 10%, n = 7) but not by its vehicle (45% ± 11%, n = 5). Propofol and its vehicle alone had no effect on the infarct size (62% ± 8% [n = 6] and 58% ± 3% [n=5], respectively). Ischemic preconditioning reduced infarct size in the absence or presence of propofol to 24% ± 7% (n = 7) and 29% ± 12% (n = 6). Desflurane-induced preconditioning markedly reduced infarct size and was blocked by propofol, whereas ischemic preconditioning was not blocked by propofol. The results suggest an important interference between propofol and anesthetic-induced preconditioning and might explain some contradictory findings in studies in humans.