What question did this study set out to answer?

This research aims to explore how lidocaine and quinidine affect action potential duration in rabbit cardiac Purkinje fibers through their action on ion channels.

January 1, 1982Circulation ResearchOpen Access

Mechanisms of action of lidocaine and quinidine on action potential duration in rabbit cardiac Purkinje fibers. An effect on steady state sodium currents?

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Population

Rabbit cardiac Purkinje fibers studied at 37 C

Comparison

Lidocaine and quinidine, as well as tetrodotoxin vs Control conditions (baseline measurements)

Design

Preclinical

Authors

TCThomas ColatskyUnited States Food and Drug Administration

Discussion

Member takes

Implication

Animal data on lidocaine versus quinidine effects caution against clinical extrapolation; leaves open human translation of these repolarization mechanisms.

Key Points

This research aims to explore how lidocaine and quinidine affect action potential duration in rabbit cardiac Purkinje fibers through their action on ion channels.
Conducted action potential and voltage clamp measurements at 37 C in rabbit cardiac Purkinje fibers.
Compared the effects of lidocaine (5 µg/ml) and quinidine on action potential duration and steady state sodium currents.
Evaluated sodium channel block using tetrodotoxin (TTX) concentrations ranging from 0.1-5 µM.
Lidocaine shortened action potential duration while quinidine lengthened it, with lidocaine showing a mean outward current of +2.3 nA and quinidine -2.1 nA.
Quinidine reduced delayed rectifier current by -68%, significantly more than lidocaine's -12% reduction.
TTX-induced sodium channel blockade confirmed that lidocaine's primary effect results from blocking TTX-sensitive sodium channels.

Structured PICO

Population

Rabbit cardiac Purkinje fibers studied at 37 C

Intervention

Lidocaine (5 µg/ml) and quinidine (5 µg/ml), as well as tetrodotoxin (TTX) (0.1-5 µM)

Comparator

Control conditions (baseline measurements)

Outcome

Action potential duration and membrane currents (holding current, delayed rectifier current, steady state sodium current)surrogate

Lidocaine shortens the cardiac action potential primarily by blocking TTX-sensitive steady-state sodium channels, whereas quinidine prolongs it by strongly depressing delayed rectifier potassium currents.

Cite This Study

Thomas Colatsky (1982) studied this question.

synapsesocial.com/papers/6a20799014cb6ef00ff48d54 https://doi.org/10.1161/01.res.50.1.17

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Implication

Animal data on lidocaine versus quinidine effects caution against clinical extrapolation; leaves open human translation of these repolarization mechanisms.

Mechanisms of action of lidocaine and quinidine on action potential duration in rabbit cardiac Purkinje fibers. An effect on steady state sodium currents?

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Mechanisms of action of lidocaine and quinidine on action potential duration in rabbit cardiac Purkinje fibers. An effect on steady state sodium currents?

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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