Depressant effects of isoflurane and halothane on isolated human atrial fibers.

The present experiments were designed to study the cellular mechanism responsible for the depressant effects of halothane and isoflurane on human atrial tissues obtained at cardiac surgery. The fibers were superfused in Tyrode's solution, and transmembrane potentials were recorded with a microelectrode technique. In atrial fibers showing fast response action potential (maximum velocity of depolarization [Vmax] greater than 100 V/s), halothane (0.75 vol%, 0.44 mM) and isoflurane (1.25 vol%, 0.53 mM) decreased slightly the upstroke velocity but depressed the plateau and twitch force significantly. In atrial fibers showing slow rate of phase-0 depolarization or when atrial fibers were depolarized in high [K]0, both halothane and isoflurane decreased the upstroke of slow response and the force. The depressant effects of anesthetics partially mimicked the actions of 1 microM tetrodotoxin and diltiazem and could be reversed by epinephrine or high [Ca]0. The delayed afterdepolarizations or aftercontractions and contracture induced by epinephrine or strophanthidin were also inhibited by both anesthetics. Halothane and isoflurane may depress normal electromechanical activity and arrhythmogenic triggered activity through a reduction of cation fluxes across the cell membrane.