The combination of catecholamines and halothane has long been recognized as arrhythmogenic. The purpose of this study was to evaluate whether the mechanism of this interaction originates at the single cell level. The incidence of spontaneous contractile waves occurring between stimulated beats (in the beat waves), early after contractions, and late after contractions was measured in rat myocytes exposed to sympathomimetics with and without halothane. Each of these endpoints in single cells has the potential to produce arrhythmias in multicellular preparations. In the beat waves and late after contractions were observed with isoproterenol (1 x 10-7 M) and norepinephrine (1-3 x 10-7 M). The incidence of these phenomena was significantly reduced in the presence of 0.30 mM halothane. Early after contractions occurred in the presence of isoproterenol (1 x 10-7 M), norepinephrine (1-3 x 10-7 M), and phenylephrine (5-10 x 10-6 M). There was a statistically significant decrease in the incidence of early after contractions in the presence of 0.30 mM halothane. These results indicate that the mechanism behind the clinically observed increased arrhythmogenicity of catecholamines with halothane does not arise at the level of single ventricular cells because halothane inhibited sympathomimetic-induced arrhythmogenic activity in this model. The probable mechanisms rather include altered impulse propagation, which might lead to phenomena such as reentry.
- anesthetics, volatile - halothane
- heart, arrhythmias - halothane
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine