Lecomte Patrick, Ouattara Alexandre, Le Manach Yannick, Landi Marc, Coriat Pierre, Riou Bruno
Laboratory of Anesthesiology, Department of Anesthesia and Critical Care, Centre Hospitalier Universitaire Pitié-Salpêtrière, Assistance-Publique-Hôpitaux de Paris, Université Pierre et Marie Curie (Paris 6), Paris, France.
Anesth Analg. 2006 Jul;103(1):9-14, table of contents. doi: 10.1213/01.ane.0000221611.02016.8c.
Remifentanil-induced hypotension may be associated with adverse ischemic myocardial events. Although these events can be easily attributed to a decrease in coronary pressure perfusion, we tested the hypothesis that remifentanil could directly affect coronary vasomotor tone. Therefore, we assessed intrinsic coronary and myocardial in vitro effects of remifentanil on a Langendorff's rabbit model and compared these effects with those provoked by similar intracoronary concentrations of sufentanil. Under general anesthesia, hearts from New Zealand rabbits were rapidly excised and mounted on an erythrocyte-perfused and isolated heart preparation. The hearts were then exposed to increasing concentrations (10-1000 nM) of either remifentanil (n = 10) or sufentanil (n = 8). Between each concentration, hearts were allowed to return to baseline status. The maximal coronary and myocardial effects of each concentration of both drugs were noted. Baseline values of coronary blood flow and myocardial performances were comparable between groups. Neither remifentanil nor sufentanil induced significant coronary and myocardial effects. These results suggest that myocardial ischemia, which may occur during remifentanil-induced hemodynamic disturbances, especially in cardiac patients, is only related to a decrease in coronary perfusion pressure provoked by peripheral hemodynamic changes.
