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Cardiovascular and cerebrovascular responses to acute hypoxia following exposure to intermittent hypoxia in healthy humans
Author(s) -
Foster Glen E.,
Brugniaux Julien V.,
Pialoux Vincent,
Duggan Cailean T. C.,
Hanly Patrick J.,
Ahmed Sofia B.,
Poulin Marc J.
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.171553
Subject(s) - hypercapnia , medicine , intermittent hypoxia , hypoxia (environmental) , nitric oxide , cerebral blood flow , blood pressure , anesthesia , cardiology , obstructive sleep apnea , acidosis , oxygen , chemistry , organic chemistry
Intermittent hypoxia (IH) is thought to be responsible for many of the long‐term cardiovascular consequences associated with obstructive sleep apnoea (OSA). Experimental human models of IH can aid in investigating the pathophysiology of these cardiovascular complications. The purpose of this study was to determine the effects of IH on the cardiovascular and cerebrovascular response to acute hypoxia and hypercapnia in an experimental human model that simulates the hypoxaemia experienced by OSA patients. We exposed 10 healthy, male subjects to IH for 4 consecutive days. The IH profile involved 2 min of hypoxia (nadir = 45.0 mmHg) alternating with 2 min of normoxia (peak = 88.0 mmHg) for 6 h. The cerebral blood flow response and the pressor responses to hypoxia and hypercapnia were assessed after 2 days of sham exposure, after each day of IH, and 4 days following the discontinuation of IH. Nitric oxide derivatives were measured at baseline and following the last exposure to IH. After 4 days of IH, mean arterial pressure increased by 4 mmHg ( P < 0.01), nitric oxide derivatives were reduced by 55% ( P < 0.05), the pressor response to acute hypoxia increased ( P < 0.01), and the cerebral vascular resistance response to hypoxia increased ( P < 0.01). IH alters blood pressure and cerebrovascular regulation, which is likely to contribute to the pathogenesis of cardiovascular and cerebrovascular disease in patients with OSA.