Key Points
- Investigate how halothane and n-alkanols alter junctional and sarcolemmal electrical properties and contractile dynamics in cardiac myocytes.
- Isolated ventricular myocytes from adult guinea pigs using whole-cell, tight-seal recording techniques.
- Applied double voltage-clamp on cell pairs and single voltage-clamp on individual cells exposed to heptanol, octanol, and halothane across -90 to +50 mV.
- Measured changes in sarcomere spacing during rest and peak systolic shortening using optical recording methods.
- Halothane and n-alkanols produced reversible electrical uncoupling between paired myocytes and reduced slope conductance across the full voltage range (-90 to +50 mV).
- Inward calcium current (Isi) showed decreased amplitude, accelerated inactivation, and a 2-3 mV hyperpolarizing shift in steady-state inactivation, while repriming kinetics remained unchanged.
- Optical measurements demonstrated increased sarcomere spacing at rest accompanied by reduced shortening during peak systole.
Structured PICO
PPopulationIsolated myocytes from adult guinea pig ventricles
IInterventionn-alkanols (heptanol, octanol) and halothane
OOutcomeElectrical properties of junctional (nexal membrane) and nonjunctional membrane (sarcolemma)surrogate
General anesthetics like n-alkanols and halothane alter membrane currents and cause electrical uncoupling in ventricular myocytes, likely via incorporation into the lipid bilayer.