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on February 3, 2005

Stroke. 2005
Published online before print February 3, 2005, doi: 10.1161/01.STR.0000155735.85888.13
A more recent version of this article appeared on March 1, 2005
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Submitted on October 26, 2004
Accepted on November 30, 2004

Effects of High Altitude Exposure on Cerebral Hemodynamics in Normal Subjects

Aurélie Van Osta BSc; Jean-Jacques Moraine PhD; Christian Mélot MD, PhD; Heimo Mairbäurl PhD; Marco Maggiorini MD, PhD; and Robert Naeije MD, PhD*

From the Laboratory of Physiology, Faculty of Medicine (A.V.O., R.N.), Laboratory of Physiology, Institute of Sports and Physiotherapy (J.J.M.), Department of Intensive Care of the Erasme Hospital (C.M.), Free University of Brussels, Belgium, Medical Clinic VII, Sports Medicine, University of Heidelberg (H.M.), Germany; and the Department of Internal Medicine of the University Hospital (M.M.), Zürich, Switzerland.

* To whom correspondence should be addressed. E-mail: rnaeije{at}ulb.ac.be.

Background and Purpose--Acute mountain sickness (AMS) may be an early stage of high altitude cerebral edema. If so, AMS could result from an alteration of dynamic autoregulation of cerebral blood flow resulting in overperfusion of capillaries and vasogenic cerebral edema.

Methods--We measured middle cerebral artery blood flow velocity (Vmca) by transcranial Doppler and arterial blood pressure by finger plethysmography at 490 m and 20 hours after arrival at 4559 m in 35 volunteers who had been randomized to tadalafil, dexamethasone, or placebo in a study on the pharmacological prevention of high altitude pulmonary edema. A dynamic cerebral autoregulation index (ARI) was calculated from continuous recordings of Vmca and blood pressure during transiently induced hypotension.

Results--Altitude was associated with an increase in a cerebral-sensible AMS (AMS-C) score (P<0.001) and with a decrease in arterial oxygen saturation (SaO2), whereas average Vmca or ARI did not change. However, at altitude, the subjects with the lowest ARI combined with the lowest SaO2 presented with the highest AMS-C score (P<0.03). In addition, a stepwise multiple linear regression analysis on arterial PCO2, SaO2, and baseline or altitude ARI identified altitude ARI as the only significant predictor of the AMS-C score (P=0.01). The AMS-C score was lower in dexamethasone-treated subjects compared with high altitude pulmonary edema-susceptible untreated subjects. Neither tadalafil nor dexamethasone had any significant effect on Vmca or ARI.

Conclusions--High altitude hypoxia is associated with impairment in the regulation of the cerebral circulation that might play a role in AMS pathogenesis.


Key words: autoregulation • cerebral blood flow • ultrasonography




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