{'fraction_non_alphanumeric': 0.037108125399872044, 'fraction_numerical': 0.022392834293026232, 'mean_word_length': 5.516666666666667, '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}}
Hindlimb unloading (HU) results in an increased predisposition to cardiac arrhythmias and changes in left ventricular (LV) connexin43 (Cx43) expression

Deconditioning produced through HU in rats, results in cardiac sympathovagal imbalance, which may increase arrhythmic risk. Reduced LV Cx43 expression and phosphorylation status may also play a role in autonomic arrhythmogenesis. We hypothesized that HU would result in an increased predisposition to spontaneous and provoked (isoproterenol 0.15mg/kg, s.c, plus brief handling/restraint) arrhythmias. We further hypothesized reduced total and increased unphosphorylated LV Cx43 expression in HU rats. Radiotelemetry probes were implanted in male, Sprague‐Dawley rats for collection of electrocardiographic data during the 10–14 day HU (n=6)/casted control (CC; n=6) protocol, at the end of the protocol in the normal posture at rest, and during an acute stressor. Arrhythmias were quantified by an established scoring method. In a separate group of HU (n=2) and CC (n=2) rats, total and unphosphorylated LV Cx43 protein expression was quantified by Western blot analysis via polyclonal and monoclonal antibodies, respectively. HU rats had significantly more spontaneous arrhythmias and a higher arrhythmic burden during an acute stressor (CC: 19±3.2 vs. HU: 51±8.2). Paradoxically, there was an increase in the phosphorylated form of LV Cx43 expression in HU as compared to CC animals. These data indicate that HU results in increased arrhythmogenesis although the cellular mechanisms remain unclear. IOER‐3726