Key result
Reducing or replacing Cx43 markedly increases spontaneous tachyarrhythmias during ischemia versus wild-type controls.
Why the study?
Little is known about the arrhythmogenic effects of transient reduction in gap junction coupling during myocardial ischemia-reperfusion.
Population
Isolated hearts from Cx43(Cre-ER(T)/fl) mice, Cx43KI32 mice, and wild-type control animals
Comparison
Reduction of Cx43 with 4-hydroxytamoxifen or replacement of Cx43 with Cx32 vs wild-type controls
Design
Preclinical study using isolated mouse hearts
Authors
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Increases ischemic tachyarrhythmias in mouse hearts with Cx43 reduction or Cx32 replacement; extends gap junction arrhythmogenicity evidence but leaves open human applicability.
p-value: p=<0.05
Reduction in gap junction channels or their conductance is arrhythmogenic during ischemia-reperfusion in isolated mouse hearts.
Sánchez‐Alcázar et al. (2011) studied Ischemia-reperfusion arrhythmias. Reduction of Cx43 with 4-OHT or replacement of Cx43 with Cx32 vs. Wild-type control animals was evaluated on Spontaneous tachyarrhythmias during ischemia (p=<0.05). Reduction of Cx43 with 4-OHT and replacement of Cx43 by Cx32 increased spontaneous tachyarrhythmias during ischemia compared to wild-type controls (52.17 and 12.29 vs 3.00; P<0.05).
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