{'fraction_non_alphanumeric': 0.021037868162692847, 'fraction_numerical': 0.008415147265077139, 'mean_word_length': 5.342222222222222, '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}}
Roles of Aortic and Carotid Chemoreceptors in Activating the Hypothalamo-Hypophyseal-Adrenocortical System During Hypoxia 1

Summary Anesthetized mongrel dogs with cannulas in the left lumboadrenal vein were subjected to hypoxia in order to determine the participation of the aortic and carotid bodies, separately and combined, in the adrenocortical response to this stressor. In intact dogs the induction of hypoxia by breathing 10% O2 at ground level for 1 hr caused rapid and sustained maximal 11-OHCS rates which paralleled the alterations in arterial oxygen, carbon dioxide and pH. On the other hand, only 3–40% of these maximal 11-OHCS rates were observed in hypoxic animals with either denervated aortic or carotid chemoreceptors. The adrenocortical response to hypoxia was abolished by denervating both aortic and carotid chemoreceptors while essentially similar changes in arterial gases and pH as those observed in intact hypoxic dogs were seen. These data demonstrate not only the necessity of functioning peripheral arterial chemoreceptors for maximal response of the hypothalamo–hypophyseal–adrenocortical system to hypoxia, but also that the aortic and carotid chemoreceptors participate equally in this response. The technical assistance of E. Blomquist, C. Lau, W. Machaj and L. Malasanos is greatly appreciated. Special thanks are due Dr. G. Courtney for her interest, assistance and review of the manuscript.