Intracellular calcium and vulnerability to fibrillation and defibrillation in Langendorff-perfused rabbit ventricles

Article

关键词: OPEN-CHEST DOGS;    UPPER LIMIT;    SHOCKS;    THRESHOLD;    ACTIVATION;    ALTERNANS;    MECHANISM;    HEART;    TRANSIENTS;    DURATION;   

DOI  :  10.1161/CIRCULATIONAHA.106.630509

来源: SCIE

【 摘 要 】

Background - The role of intracellular calcium (Ca-i) in defibrillation and vulnerability is unclear. Methods and Results - We simultaneously mapped epicardial membrane potential and Ca-i during shock on T-wave episodes (n = 104) and attempted defibrillation episodes ( n = 173) in 17 Langendorff-perfused rabbit ventricles. Unsuccessful and type B successful defibrillation shocks were followed by heterogeneous distribution of Ca-i, including regions of low Ca-i surrounded by elevated Ca-i (Ca-i sinkholes) 31 +/- 12 ms after shock. The first postshock activation then originated from the Ca-i sinkhole 53 +/- 14 ms after the shock. No sinkholes were present in type A successful defibrillation. A Ca-i sinkhole also was present 39 +/- 32 ms after a shock on T that induced ventricular fibrillation, followed 22 +/- 15 ms later by propagated wave fronts that arose from the same site. This wave propagated to form a spiral wave and initiated ventricular fibrillation. Thapsigargin and ryanodine significantly decreased the upper limit of vulnerability and defibrillation threshold. We studied an additional 7 rabbits after left ventricular endocardial cryoablation, resulting in a thin layer of surviving epicardium. Ca-i sinkholes occurred 31 +/- 12 ms after the shock, followed in 19 +/- 7 ms by first postshock activation in 63 episodes of unsuccessful defibrillation. At the Ca-i sinkhole, the rise of Ca-i preceded the rise of epicardial membrane potential in 5 episodes. Conclusions - There is a heterogeneous postshock distribution of Ca-i. The first postshock activation always occurs from a Ca-i sinkhole. The Ca-i prefluorescence at the first postshock early site suggests that reverse excitation-contraction coupling might be responsible for the initiation of postshock activations that lead to ventricular fibrillation.

【 授权许可】

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