{'fraction_non_alphanumeric': 0.05935483870967742, 'fraction_numerical': 0.06516129032258064, 'mean_word_length': 5.05859375, 'pattern_counts': {'":': 0, '<': 4, '<?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}}
e0092 AVE0991 improves left ventricular remodelling and cardiac function induced by myocardial infarction in rats

Objective To evaluate the effects of 4-week treatment with the nonpeptide angiotensin-(1-7) analogue AVE 0991 on heart function and left ventricular remodelling induced by myocardial infarction (MI). Methods In this study, we evaluated the cardiac effects of AVE 0991 on normal and infracted male Sprague-Dawley (SD) rats. MI was induced by left coronary artery ligation. After 4 weeks of treatment, transthoracic echocardiography (TTE) was used to evaluate cardiac function. The heart wet weight was recorded, normalised for body weight. Left ventricle serial sections were dyed with triphenyltetrazolium chloride (TTC) stain to quantify the infarct size, with Masson's trichrome stain to quantify collagen volume fraction (CVF), and with haematoxylin-eosin (HE) stain for diameter measurement of cardiomyocytes. Results Infarct size was slightly reduced in AVE 0991 group compared to control group (42.6±3.6% vs 50.9±4.4%, p<0.01). In addition, AVE 0991 treatment attenuated the decrease in LVFS (25.54±7.33% vs 18.41±3.32%, p<0.05) and LVEF (54.82±11.63% vs 42.7±6.5%, p<0.05) compared to control group. AVE 0991 also reduced MI-induced hypertrophy as quantified by diameter measurements of cardiomyocytes (vs. control group 25.49±4.37 μm vs 32.06±6.85 μm, p<0.05). Conclusion The nonpeptide angiotensin-(1-7) analogue AVE 0991 has a cardioprotective effect on impairment of heart function and ventricular remodelling induced by MI.