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Cardiovascular and respiratory profiles during the sleep–wake cycle of rats previously submitted to chronic intermittent hypoxia
Author(s) -
Bazilio Darlan S.,
Bonagamba Leni G. H.,
Moraes Davi J. A.,
Machado Benedito H.
Publication year - 2019
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep087784
Subject(s) - cardiorespiratory fitness , intermittent hypoxia , medicine , hypoxia (environmental) , respiratory system , ventilation (architecture) , heart rate , endocrinology , anesthesia , apnea , plethysmograph , cardiology , blood pressure , obstructive sleep apnea , chemistry , oxygen , mechanical engineering , organic chemistry , engineering
New FindingsWhat is the central question of this study? Chronic intermittent hypoxia (CIH) causes increased arterial pressure (AP), sympathetic overactivity and changes in expiratory modulation of sympathetic activity. However, changes in the short‐term sleep–wake cycle pattern after CIH and their potential impact on cardiorespiratory parameters have not been reported previously.What is the main finding and its importance? Exposure to CIH for 10 days elevates AP in wakefulness and sleep but does not cause major changes in short‐term sleep–wake cycle pattern. A higher incidence of muscular expiratory activity was observed in rats exposed to CIH only during wakefulness, indicating that active expiration is not required for the increase in AP in rats submitted to CIH.Abstract Chronic intermittent hypoxia (CIH) increases arterial pressure (AP) and changes sympathetic–respiratory coupling. However, the alterations in the sleep–wake cycle after CIH and their potential impact on cardiorespiratory parameters remain unknown. Here, we evaluated whether CIH‐exposed rats present changes in their short‐term sleep–wake cycle pattern and in cardiorespiratory parameters. Male Wistar rats (∼250 g) were divided into CIH and control groups. The CIH rats were exposed to 8 h day −1 of cycles of normoxia (fraction of inspired O 2 = 0.208, 5 min) followed by hypoxia (fraction of inspired O 2 = 0.06, 30–40 s) for 10 days. One day after CIH, electrocorticographic activity, cervical EMG, AP and heart rate were recorded for 3 h. Plethysmographic recordings were collected for 2 h. A subgroup of control and CIH rats also had the diaphragm and oblique abdominal muscle activities recorded. Chronic intermittent hypoxia did not alter the time for sleep onset, total time awake, durations of rapid eye movement (REM) and non‐REM (NREM) sleep and number of REM episodes in the 3 h recordings. However, a significant increase in the duration of REM episodes was observed. The AP and heart rate were increased in all phases of the cycle in rats exposed to CIH. Respiratory frequency and ventilation were similar between groups in all phases, but tidal volume was increased during NREM and REM sleep in rats exposed to CIH. An increase in the incidence of active expiration during wakefulness was observed in rats exposed to CIH. The data show that CIH‐related hypertension is not caused by changes in the sleep–wake cycle and suggest that active expiration is not required for the increase in AP in freely moving rats exposed to CIH.