Imaging arrhythmogenic calcium signaling in intact hearts.

Pediatric Cardiology
Peng-Sheng ChenShien-Fong Lin

Abstract

Protein complex of the cardiac junctional sarcoplasmic reticulum (SR) membrane formed by type 2 ryanodine receptor, junction, triadin, and calsequestrin is responsible for controlling SR calcium (Ca) release. Increased intracellular calcium (Ca(i)) activates the electrogenic sodium-Ca exchanger current, which is known to be important in afterdepolarization and triggered activities (TAs). Using optical-mapping techniques, it is possible to simultaneously map membrane potential (V (m)) and Ca(i) transient in Langendorff-perfused rabbit ventricles to better define the mechanisms by which V (m) and Ca(i) interactions cause early afterdepolarizations (EADs). Phase 3 EAD is dependent on heterogeneously prolonged action potential duration (APD). Electrotonic currents that flow between a persistently depolarized region and its recovered neighbors underlies the mechanisms of phase 3 EADs and TAs. In contrast, "late phase-3 EAD" is induced by APD shortening, not APD prolongation. In failing ventricles, upregulation of apamin-sensitive Ca-activated potassium (K) channels (I(KAS)) causes APD shortening after fibrillation-defibrillation episodes. Shortened APD in the presence of large Ca(i) transients generates late-phase 3 EADs and recurre...Continue Reading

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Citations

Dec 15, 2015·Journal of the American Heart Association·Shuenn-Nan ChiuJiunn-Lee Lin
Mar 27, 2016·American Journal of Physiology. Heart and Circulatory Physiology·Rafael JaimesMatthew W Kay
Dec 23, 2016·Clinical Medicine Insights. Cardiology·Peter Baumeister, T Alexander Quinn

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