What question did this study set out to answer?

To determine the electrophysiological mechanisms and kinetics responsible for quinidine-induced depression of maximum upstroke velocity in cardiac tissue.

March 1, 1982Circulation ResearchOpen Access

Mechanisms of quinidine-induced depression of maximum upstroke velocity in ovine cardiac Purkinje fibers.

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Authors

FWFrancis M. WeldHighland Hospital JCJames CoromilasElectrophysiology JRJeffrey N. RottmanUniversity of Maryland, Baltimore

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Implication

In vitro support for quinidine Na-channel model; leaves open translation to clinical antiarrhythmic use.

Key Points

To determine the electrophysiological mechanisms and kinetics responsible for quinidine-induced depression of maximum upstroke velocity in cardiac tissue.
Applied a double microelectrode voltage clamp technique to ovine cardiac Purkinje fibers to manipulate transmembrane voltage and deliver conditioning electrical pulses.
Evaluated the relationship between maximum upstroke velocity and transmembrane voltage across stimulation drive cycles ranging from 500 milliseconds to 20 seconds.
Quinidine blockade increased as transmembrane voltage became more positive from -60 to +40 mV, while drug dissociation rates increased as voltage shifted more negative from -60 to -140 mV.
The relationship between maximum upstroke velocity and voltage matched a model featuring voltage-dependent binding and unbinding rate constants without the previously proposed -40-mV shift in inactivation kinetics.

Cite This Study

Weld et al. (1982) studied this question.

synapsesocial.com/papers/6a83423ddd3eabac52f2b126 https://doi.org/10.1161/01.res.50.3.369

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Mechanisms of quinidine-induced depression of maximum upstroke velocity in ovine cardiac Purkinje fibers.

Discussion

Member takes

Implication

Key Points

Cite This Study

Mechanisms of quinidine-induced depression of maximum upstroke velocity in ovine cardiac Purkinje fibers.

Discussion

Member takes

Implication

Key Points

Cite This Study

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