Halothane antagonizes ouabain toxicity in isolated canine Purkinje fibers.

Standard intracellular microelectrode techniques were used to study the effects of halothane on ouabain-induced delayed after depolarizations (DAD) in canine Purkinje fibers. Free running Purkinje fibers were superfused with 2 X 10(-7)M ouabain in Krebs-Henseleit buffer for 30-50 min until DAD appeared. Purkinje fibers were then paced for 20 beats at cycle lengths between 1,000 ms and 200 ms, and the amplitude of the DAD and coupling interval between the DAD and last paced beat were determined. Halothane (0.5, 1, and 2%) was then administered and measurements repeated. Halothane produced dose-related decreases in DAD amplitude without changing DAD coupling interval. The ability of calcium to antagonize the effects of halothane was evaluated by doubling buffer calcium concentration to 5 mM in the presence of halothane 2%. Doubling buffer calcium concentration to 5 mM antagonized the reduction of DAD amplitude caused by halothane. In several preparations, dysrhythmias occurred during ouabain superfusion. Halothane reversibly terminated these arrhythmias. Halothane antagonizes DAD and dysrhythmias induced in vitro by ouabain toxicity. This effect, in part, may account for the apparent effectiveness of halothane against ouabain-induced dysrhythmias in vivo.