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December 1, 2000Journal of Cardiovascular Pharmacology16 citations

Role of Sodium Channels in Ventricular Fibrillation: A Study in Nonischemic Isolated Hearts

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Population

Nonischemic isolated feline hearts (n=14) and nonischemic isolated rabbit hearts (n=4)

Comparison

Sodium channel blockers: tetrodotoxin (5 x 10 M)… vs Nontreated hearts (baseline before application)

Design

Preclinical

Authors

GAGiora AmitzurWSWolfgang SchoelsAVAlexander Visokovsky

Discussion

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Overview

No immediate implications for clinical VF management; hypothesis-generating for sodium channel contributions to arrhythmia organization.

Structured PICO

P
Population
Nonischemic isolated feline hearts (n=14) and nonischemic isolated rabbit hearts (n=4)
I
Intervention
Sodium channel blockers: tetrodotoxin (5 x 10(-7) M) or lidocaine (1 x 10(-5) M)
C
Comparator
Nontreated hearts (baseline before application)
O
Outcome
Electrophysiologic parameters including epicardial conduction time, refractoriness, fastest rate for 1:1 pacing/response capture, tissue resistivity, peak frequency, normalized entropy, and spontaneous arrhythmia terminationsurrogate

Sodium channel blockade in isolated hearts slows conduction time and increases arrhythmia organization, suggesting sodium channels actively maintain ventricular fibrillation.

Cite This Study

Amitzur et al. (2000) studied this question.

synapsesocial.com/papers/6a1b11a0c276bea67e0c7322https://doi.org/10.1097/00005344-200012000-00015
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