RESUMO
BACKGROUND: The purpose of this study is to examine the effect of Desflurane on myocardial contractility and cellular electrophysiologic behabior in isolated guinea pig and rat right ventricular papillary muscle. METHODS: The isometric force of a guinea pig ventricular papillary muscle was studied in normal and 26 mM Tyrode's solution at various stimulation rates. Experiments using rat papillary muscles under normal Tyrode's solution at resting-state (RS) and using guinea pig papillary muscles under low Na Tyrode's solution (25 mM) were performed to evaluate the effect on Ca2+ release from the sarcoplasmic reticulum (SR). Normal and slow action potentials (APs) were evaluated by using a conventional microelectrode technique. Effects of desflurane on SR function in situ were examined by its effect on rapid colling contractures (RCCs). 1 MAC (end-tidal concentration: 6%) and 2 MAC desflurane were applied. RESULTS: Desflurane equivalent to 6% and 12% depressed guinea pig myocardial contractions in the control to -70% and -40% from RS to 3 Hz stimulation rates. Contractile force after rest in rat and guinea pig myocardium under low Na Tyrode's solution showed modest depression. In the partially depolarized, beta-adrenergically stimulated myocardium, 6% and 12% desflurane caused marked depression of late force (6%: -60%, 12%: -80%) with moderate changes of early peak force (6%: -20%, 12%: -40%). RCCs were abolished at 6% concentration. CONCLUSIONS: The direct myocardial depressant effects of desflurane is slightly greater to those seen with isoflurane. The rapid initial release of Ca2+ from the SR by depolarization seems to be modestly depressed, although certain release pathways induced by rapid colling appear to be markedly depressed.