Anesthetic‐Induced Preconditioning Is Inhibited By The Hypnotic Agent Propofol

Reactive oxygen species (ROS) are part of the signal transduction pathway of ischemic and anesthetic‐induced myocardial preconditioning 1 , 2 . Propofol due to its ROS scavenging properties might interfere with signal transduction of preconditioning 3 . We tested the hypothesis, that ischemic and desflurane (DES)‐induced preconditioning (PC) is blocked by propofol. All experiments conformed to APS and NIH guidelines. Pentobarbital‐anesthetized rabbits (n=39) were instrumented and subjected to 30‐min coronary artery occlusion and 3 h of reperfusion. Rabbits were randomized to 6 separate groups: 0.0 or 1.0 MAC desflurane (30 min duration, 30 min memory period) or ischemic PC (5 min ischemia with 30 min memory period) in the absence or presence of propofol (10 mg/kg/h iv). Statistics: One‐ and two‐way ANOVA with posthoc Duncan test. Data are mean±SEM. Infarct size (IS) was 59±2% of area at risk (IS/AAR) in control experiments. DES significantly (*p<0.05) reduced IS to 35±2%*. Propofol alone had no effect on IS (62±3%) but blocked DES‐induced PC (65±4%). Ischemic PC reduced IS in the absence or presence of propofol to 24±3%* and 29±5%* respectively. DES‐induced PC markedly reduced myocardial infarct size and was blocked by the ROS scavenger propofol. Single cycle ischemic preconditioning (IPC) markedly reduced infarct size and was not blocked by propofol. The results suggest important differences in levels of ROS production between IPC and APC. Acknowledgement This study was supported in part by funds from the IZKF, Wuerzburg and Baxter, Germany.