{'fraction_non_alphanumeric': 0.029787234042553193, 'fraction_numerical': 0.023404255319148935, 'mean_word_length': 5.243362831858407, 'pattern_counts': {'":': 0, '<': 4, '<?xml version=': 0, '>': 1, '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}}
[Changes in expression of angiotensin subtype AT1A and AT2 receptors in rats during cardiac remodeling following myocardial infarction].

Immunohistochemical and electron microscopic techniques and image analysis were employed to investigate the regulation of cardiac AT1A and AT2 subtype receptors in rats during cardiac remodeling following myocardial infarction (MI). Positive immunostaining for AT1A and AT2 receptors was observed in myocytes and vessels with AT1A being more than AT2. Three days after MI, disappearance of myocardial cross striation and fibroblast hyperplasia were found with electron microscopy. AT1A receptor protein expression in myocardial noninfarcted portion notably increased compared with that in sham-operated control rats (P < 0.001). No apparent changes were observed in AT2 receptor (P > 0.05). Two weeks after MI, myocyte cross striation and collagen deposition were found. Meanwhile, AT1A receptor staining decreased compared with that of three days after MI (P < 0.01), but there was still more than that of the control (P < 0.05). AT2 receptor was significantly increased compared with that of the sham-operated control rats (P < 0.001). These results suggest that both AT1A and AT2 receptor protein expression was upregulated in noninfarcted myocardium after MI, and the regulation of AT1A and AT2 receptors after MI may be involved in post-infarction cardiac remodeling.