{'fraction_non_alphanumeric': 0.029450261780104712, 'fraction_numerical': 0.017015706806282723, 'mean_word_length': 5.73568281938326, 'pattern_counts': {'":': 0, '<': 2, '<?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}}
Alterations in cardiac connexin 43 and microvessel prevalence with ventricular performance deficits during murine diabetic cardiomyopathy

Non‐ischemic cardiomyopathy is a common complication in type 1 diabetic patients. The mechanisms involved are unclear. We tested the hypothesis that changes in microvascular prevalence and alterations in connexin (Cx) isoforms are contributors. A single dose of streptozotocin (STZ, 150mg/kg) was used to induce type‐1 diabetes in a mouse model. Echocardiography and ECGs were performed at 1‐ and 5‐week. Cardiac tissue was isolated for histochemistry. LV fractional shortening and cardiac output were reduced in STZ treated mice relative to controls (p<0.05). QTc was prolonged, with no change in ST segment, in these mice. Immunostaining for CD31 demonstrated a 35% reduction in microvessels/myocardial area (p<0.01), which was highly correlated to FS%. These changes were also associated with increased protein 3‐nitrotyrosine. Cx43 distribution was changed post‐STZ, as Cx43 was dispersed from intercalated disks where it supports the longitudinal and transverse spread of the action potential. In contrast, Cx40 distribution was unchanged relative to controls throughout the study. These data demonstrate that this diabetic mouse model has hallmark features observed in humans with respect to non‐ischemic contractile alterations, electrophysiological abnormalities, and microvasculare rarefaction. Reactive nitrogen species and alterations in gap junction channels might be involved.