{'fraction_non_alphanumeric': 0.039927404718693285, 'fraction_numerical': 0.007259528130671506, 'mean_word_length': 6.885714285714286, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Intracellular Calcium Dynamics, Shortened Action Potential Duration, and Late‐Phase 3 Early Afterdepolarization in Langendorff‐Perfused Rabbit Ventricles

Calcium Dynamics, APD Shortening, and Late‐Phase 3 EAD. Introduction: To elucidate the mechanism of late‐phase 3 early after depolarization (EAD) in ventricular arrhythmogenesis, we hypothesized that intracellular calcium (Cai) overloading and action potential duration (APD) shortening may promote late‐phase 3 EAD and triggered activity, leading to development of ventricular fibrillation (VF).