Sevoflurane exerts a dual, voltage-dependent effect on the inward rectifier potassium current in guinea pig ventricular cardiomyocytes, which is modulated by intracellular magnesium and polyamines.
Answers are grounded in this paper and cite their sources.
Sevoflurane may influence ventricular repolarization via IK1; leaves open clinical relevance pending human studies.
The effects of sevoflurane on the inward rectifier potassium current (IKIR) were examined in guinea pig ventricular cardiomyocytes using the whole cell patch-clamp methodology. Sevoflurane had a unique dual effect on the steady-state current amplitude, producing a reversible, concentration- and voltage-dependent block of the inward current at potentials negative to the potassium equilibrium potential (EK) but enhancing the outward current positive to EK. Accordingly, the steady-state conductance negative to EK was reduced by sevoflurane, but conductance positive to EK was increased. The chord conductance-voltage relationship showed depolarizing shifts at 0.7, 1.3, and 1.6 mM sevoflurane. When the myocytes were dialyzed with 10 mM Mg2+, but not with 1.0 mM Mg2+, sevoflurane further slowed current activation kinetics. With 10 mM intracellular Mg2+, the outward current enhancement by sevoflurane and the associated shifts in half-activation potential were abolished. Polyamines abolished all effects of sevoflurane on IKIR. With the use of the Woodhull model for voltage-dependent block, we determined the sevoflurane interaction site with the inward rectifier potassium channel to be at an electrical distance of 0.2 from the extracellular side.
No takes yet. Share an insight, caveat, or question.
Stadnicka et al. (1997) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: