{'fraction_non_alphanumeric': 0.00972972972972973, 'fraction_numerical': 0.0075675675675675675, 'mean_word_length': 5.9849056603773585, '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}}
Effects of Increased Myocardial Oxygen Consumption on Coronary Reactive Hyperemia in the Awake Dog

This study was undertaken to determine whether coronary reactive hyperemia is coupled to myocardial metabolic activity and thus proportional to myocardial oxygen consumption or whether it is mechanically determined, resulting from direct myogenic relaxation of coronary vascular smooth muscle in response to loss of the stretch stimulus provided by arterial blood pressure. In ten unanesthetized dogs, coronary artery occlusions 1–7 seconds in duration produced reactive hyperemia resulting in 260–420% repayment of the blood flow debt incurred during occlusion. When myocardial oxygen consumption and coronary blood flow were increased by paired ventricular stimulation, reactive hyperemia increased to a commensurate degree so that debt repayments remained unchanged at 270–420%. That this augmentation of reactive hyperemia was actually related to increased myocardial metabolic activity during the occlusion was demonstrated by a similar increase in the hyperemic response when paired ventricular stimulation was applied during the occlusion only. To demonstrate that augmented reactive hyperemia during paired ventricular stimulation did not merely represent direct myogenic relaxation imposed on a vascular bed more dilated from the onset, coronary blood flow was increased by infusion of adenosine with no increase in myocardial oxygen consumption. During adenosine infusion, the total volume of reactive hyperemic blood flow was similar to that observed during the control situation. Thus, in the coronary system reactive hyperemia is related to myocardial metabolic activity during the interval of arterial occlusion and not influenced by alterations in resting coronary blood flow which occur independently of myocardial oxygen consumption.