Abstract
In their letter, Wolkowicz et al . raise a valid point questioning whether other effects of 2-aminoethoxydiphenyl borate (2-APB) might also have contributed to ventricular fibrillation (VF) initiation, especially its effects on voltage-independent calcium channels, as was also mentioned in the Discussion section of our manuscript recently published in Cardiovascular Research .1 In this study, we showed that prolonging the minimal action potential duration (APD) can decrease the complexity (e.g. number of rotors) during sustained VF. To induce fibrillation in neonatal rat ventricular cardiomyocyte monolayers and in adult rat hearts, we used 2-APB. We postulated that the re-entrant conduction patterns resembling VF after 2-APB treatment could be partly attributed to the effect of 2-APB on gap junctional coupling.2 The main purpose of our study was to study the maintenance properties of VF. Going into length on the mechanism by which 2-APB induces VF would …
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