{'fraction_non_alphanumeric': 0.012804097311139564, 'fraction_numerical': 0.012163892445582587, 'mean_word_length': 5.153543307086614, '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}}
Intramyocardial gas tensions in the canine heart.

Intramyocardial gas tensions were determined in the left ventricular wall of the canine heart by means of chronically implanted silastic tonometers. In the central zone of the myocardial wall the mean baseline PO2 was 22 mmHg and the mean baseline PCO2 28 mmHg. Breathing of pure oxygen elevated the myocardial PO2 to a level of 60 to 90 mmHg. Hypovolaemic shock induced by shedding 30% of the blood volume resulted in a sharp decrease of the myocardial PO2 and a marked increase of the myocardial PCO2. During hypovolaemia, ventilation with pure oxygen elevated the oxygen tension to the control level and, after re-infusion of the shed blood, the response of the myocardial PO2 to oxygen breathing became higher than normal. Correction of hypovolaemic with a plasma expander Haemaccel restored the myocardial oxygen tension to the baseline level. Ligation of the left anteior descending coronary artery produced a rapid fall of PO2 and a profound increase of PCO2 in the corresponding myocardial area. After coronary ligation, developing tissue ischaemia usually resulted in ventricular fibrillation within a few minutes. Cardiac massage was started immediately, but produced no correction of tissue gas tensions, although the arterial blood gases remained normal. Ligation of the right coronary artery or the left circumflex coronary artery for short periods increased the myocardial PO2 in the vicinity of the left anterior descending branch, probably due to reactive hyperaemia around the ischaemic tissue.