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Published Online
on October 13, 2005

Stroke. 2005
Published online before print October 13, 2005, doi: 10.1161/01.STR.0000185923.49484.0f
A more recent version of this article appeared on November 1, 2005
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Submitted on April 29, 2005
Revised on June 15, 2005
Accepted on July 11, 2005

Overnight Changes in the Cerebral Vascular Response to Isocapnic Hypoxia and Hypercapnia in Healthy Humans. Protection Against Stroke

Guy E. Meadows PhD; Futoshi Kotajima PhD; Ali Vazir MBBS; Konstantinos Kostikas PhD; Anita K. Simonds MD; Mary J. Morrell PhD; and Douglas R. Corfield PhD*

From the Clinical and Academic Unit of Sleep and Breathing (G.E.M., F.K., A.V., K.K., A.K.S., M.J.M., D.R.C.), National Heart and Lung Institute, Imperial College, London, U.K.; Institute of Science and Technology in Medicine (D.R.C.), School of Life Sciences, Keele University, Keele, U.K.; and the Sleep and Ventilation Unit (G.E.M., F.K., A.V., K.K., A.K.S., M.J.M.), Royal Brompton Hospital, London, U.K.

* To whom correspondence should be addressed. E-mail: d.corfield{at}keele.ac.uk.

Background and Purpose--The reduction in hypercapnic cerebral vascular reactivity that occurs in the morning after sleep is associated with an increased risk of cerebral ischemia and stroke. It is not known if the cerebral vascular response to hypoxia is similarly reduced in the morning, but such a reduction could be considered a further risk factor for cerebral vascular disease.

Methods--To test if the cerebral vascular response to hypoxia is reduced in the morning, the overnight changes in the left middle cerebral artery velocity (MCAV) in response to isocapnic hypoxia (IH) and hypercapnia before and after a normal night sleep were determined in 18 individuals.

Results--From evening to morning, hypercapnic cerebral vascular reactivity decreased significantly (evening 2.0±0.4, morning 1.3±0.2 cm/sec/mm Hg; P<0.05); in contrast, the increase in MCAV in response to IH (-10% SaO2) was unchanged (evening 9.0±1.4, morning 8.7±2.2%; P>0.05).

Conclusions--Our findings indicate that substantial differences exist in the regulation of the cerebral circulation in response to hypoxia and hypercapnia on waking from sleep. An intact cerebral vascular response to IH, during this time period, could be interpreted as a protective mechanism against cerebral ischemia and stroke; this is of particular relevance to patients with obstructive sleep apnea who arouse from sleep during hypoxia.


Key words: cerebral blood flow • hypercapnia • isocapnic hypoxia • middle cerebral artery velocity • nitric oxide • physiology • transcranial Doppler




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