September 1, 1991Circulation ResearchOpen Access

Blockade of cardiac sodium channels by amitriptyline and diphenylhydantoin. Evidence for two use-dependent binding sites.

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Population

Isolated rabbit atrial and ventricular myocytes

Comparison

Amitriptyline and diphenylhydantoin individually… vs Lidocaine; varying extracellular and…

Design

Preclinical

Authors

MBMichael BarberBrigham Young University CSC F StarmerElectrophysiology AGAugustus O. GrantDuke Medical Center

Discussion

Member takes

Implication

Questions mechanism of diphenylhydantoin reversal in amitriptyline toxicity; leaves open distinct sodium channel sites for further study.

Structured PICO

Population

Isolated rabbit atrial and ventricular myocytes

Intervention

Amitriptyline (0.4 microM) and diphenylhydantoin (10-80 microM) individually and in combination

Comparator

Lidocaine; varying extracellular (pHo) and intracellular (pHi) pH levels

Outcome

Sodium current block and time constant of recovery (tau r)surrogate

Amitriptyline and diphenylhydantoin block cardiac sodium channels via two distinct use-dependent binding sites, challenging the belief that diphenylhydantoin reverses amitriptyline toxicity through direct competition.

Cite This Study

Barber et al. (1991) studied this question.

synapsesocial.com/papers/6a7728ffd2fa2470761eaeab https://doi.org/10.1161/01.res.69.3.677

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Blockade of cardiac sodium channels by amitriptyline and diphenylhydantoin. Evidence for two use-dependent binding sites.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Blockade of cardiac sodium channels by amitriptyline and diphenylhydantoin. Evidence for two use-dependent binding sites.

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider