{'fraction_non_alphanumeric': 0.014245014245014245, 'fraction_numerical': 0.002136752136752137, 'mean_word_length': 6.5133689839572195, '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}}
Role of Cardiac Sympathetic Nerves in the Genesis of Myocardial Ischemia Distal to Coronary Stenoses

This manuscript summarizes the effects of cardiac sympathetic nerve activation on coronary blood flow and myocardial function, metabolism, and morphology distal to stenoses. Whereas cardiac sympathetic nerve activation induces an increase in myocardial function and metabolism accompanied by metabolic coronary dilation under physiological conditions, this response is different in the presence of coronary stenoses. With decreasing coronary hyperemic reserve, distal to an increasing degree of coronary stenosis, the predominant response to sympathetic stimulation is continuously shifted from metabolic dilation to α-adrenergic vasoconstriction. With a severe coronary stenosis, both electrical stimulation of cardiac sympathetic nerves and reflex sympathetic activation by carotid occlusion induce poststenotic vasoconstriction and ischemia of the dependent myocardium. Poststenotic vasoconstriction is mediated by vascular α2-adrenoceptors and is prevented by phentolamine, rauwolscine, and nifedipine. Prolonged sympathetic activation even results in patchy subendocardial necroses. There is a vicious cycle between poststenotic vasoconstriction, myocardial ischemia,-and cardiac sympathetic nerve activity that results in a progressive perfusion impairment during 20 min severe coronary stenosis.