What question did this study set out to answer?

To examine the kinetic properties and state dependence of cardiac sodium channel block by amiodarone compared to lignocaine in single isolated ventricular myocytes.

March 1, 1991British Journal of PharmacologyOpen Access

Block of cardiac sodium channels by amiodarone studied by using of action potential in single ventricular myocytes

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Why the study?

Does amiodarone block cardiac sodium channels in ventricular myocytes isolated from guinea-pig hearts compared to lignocaine?

Population

Ventricular myocytes isolated from guinea-pig hearts

Comparison

Amiodarone (1 microM) vs Lignocaine (40 microM)

Design

Preclinical

Authors

HHHaruo HonjoHealth Promotion Agency IKItsuo KodamaNagoya University KKKaichiro KamiyaNagoya University

Discussion

Member takes

Implication

Should not change amiodarone use; leaves open translation of inactivated-state Na block to human antiarrhythmic efficacy.

Key Points

To examine the kinetic properties and state dependence of cardiac sodium channel block by amiodarone compared to lignocaine in single isolated ventricular myocytes.
Isolated ventricular myocytes from guinea-pig hearts and performed whole-cell current-clamp and voltage-clamp recordings using suction pipette electrodes.
Used the maximum upstroke velocity (Vmax) of the action potential as a qualitative measure of sodium channel availability under baseline, depolarizing conditioning clamps, and variable recovery intervals with amiodarone (1 µM) or lignocaine (40 µM).
Tonic block was minimal at 0.03 Hz, with reference action potential Vmax decreasing by only 6% to 11% under amiodarone or lignocaine.
Depolarization induced rapid channel block, with onset time constants at 0 mV clamp measuring 25 ms for amiodarone versus 122 ms for lignocaine.
Recovery of Vmax followed a dual exponential function, with late slow time constants (tau R) at resting potential of 418 ms for amiodarone and 178 ms for lignocaine, which shortened voltage-dependently upon hyperpolarization.

Structured PICO

Does amiodarone block cardiac sodium channels in ventricular myocytes isolated from guinea-pig hearts compared to lignocaine?

Population

Ventricular myocytes isolated from guinea-pig hearts

Intervention

Amiodarone (1 microM)

Comparator

Lignocaine (40 microM)

Outcome

Maximum upstroke velocity (Vmax) of the action potentialsurrogate

Amiodarone exhibits rapid onset and offset block of cardiac sodium channels primarily in the inactivated state, similar to lignocaine, contributing to its antiarrhythmic properties.

Cite This Study

Honjo et al. (1991) studied this question.

synapsesocial.com/papers/6a7163a0f44fa9f079df2fda https://doi.org/10.1111/j.1476-5381.1991.tb12228.x

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Block of cardiac sodium channels by amiodarone studied by using of action potential in single ventricular myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Block of cardiac sodium channels by amiodarone studied by using of action potential in single ventricular myocytes

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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