Repetitive apneas induce periodic hypertension in normal subjects through hypoxia

• Published in: Journal of applied physiology (1985) Vol. 72; no. 3; p. 821
• Main Authors: van den Aardweg, J G, Karemaker, J M
• Format: Journal Article
• Language: English
• Published: United States 01.03.1992
• Subjects: Adult; Atropine - pharmacology; Blood Pressure - physiology; Chemoreceptor Cells - physiopathology; Heart Rate - physiology; Humans; Hypertension - etiology; Hypertension - physiopathology; Hypoxia - complications; Hypoxia - physiopathology; Male; Oxygen; Sleep Apnea Syndromes - complications; Sleep Apnea Syndromes - physiopathology
• ISSN: 8750-7587
• DOI: 10.1152/jappl.1992.72.3.821

Periodic increases in blood pressure (BP) can occur in the sleep apnea syndrome (SAS) during recurrent apneas. To investigate the mechanisms causing this periodic hypertension, we simulated SAS by imposing a matching breathing pattern on seven healthy awake male volunteers. Continuous finger arterial BP, electrocardiogram, arterial O2 saturation (SaO2), end-tidal CO2, and tidal volume were measured. The role of hypoxia was studied by comparing apneas during depletion of O2 in the spirometer with those during 100% O2 breathing. In all subjects, BP periodically reached values greater than 150/95 mmHg in the hypoxic series. During the hyperoxic apnea series, however, BP remained stable. End-apneic mean BP was shown to be inversely correlated to SaO2 in six subjects in the SaO2 range from 60 to 100%. Although the hypoxic BP pattern closely mimicked that in SAS, the heart rate pattern in four of our subjects remained distinct from that in patients. Atropine could not prevent large BP swings in the hypoxic series. We conclude that SaO2 is a major determinant of periodic hypertension in recurrent apneas. Its effect probably results from chemoreflex modulation of peripheral resistance.