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- Aurélie Van Osta
- 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.
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- Jean-Jacques Moraine
- 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.
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- Christian Mélot
- 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.
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- Heimo Mairbäurl
- 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.
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- Marco Maggiorini
- 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.
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- Robert Naeije
- 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.
説明
<jats:p> <jats:bold> <jats:italic>Background and Purpose—</jats:italic> </jats:bold> 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. </jats:p> <jats:p> <jats:bold> <jats:italic>Methods—</jats:italic> </jats:bold> We measured middle cerebral artery blood flow velocity ( <jats:italic>V</jats:italic> mca) 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 <jats:italic>V</jats:italic> mca and blood pressure during transiently induced hypotension. </jats:p> <jats:p> <jats:bold> <jats:italic>Results—</jats:italic> </jats:bold> Altitude was associated with an increase in a cerebral-sensible AMS (AMS-C) score ( <jats:italic>P</jats:italic> <0.001) and with a decrease in arterial oxygen saturation (Sa <jats:sc>o</jats:sc> <jats:sub>2</jats:sub> ), whereas average <jats:italic>V</jats:italic> mca or ARI did not change. However, at altitude, the subjects with the lowest ARI combined with the lowest Sa <jats:sc>o</jats:sc> <jats:sub>2</jats:sub> presented with the highest AMS-C score ( <jats:italic>P</jats:italic> <0.03). In addition, a stepwise multiple linear regression analysis on arterial P <jats:sc>co</jats:sc> <jats:sub>2</jats:sub> , Sa <jats:sc>o</jats:sc> <jats:sub>2</jats:sub> , and baseline or altitude ARI identified altitude ARI as the only significant predictor of the AMS-C score ( <jats:italic>P</jats:italic> =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 <jats:italic>V</jats:italic> mca or ARI. </jats:p> <jats:p> <jats:bold> <jats:italic>Conclusions—</jats:italic> </jats:bold> High altitude hypoxia is associated with impairment in the regulation of the cerebral circulation that might play a role in AMS pathogenesis. </jats:p>
収録刊行物
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- Stroke
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Stroke 36 (3), 557-560, 2005-03
Ovid Technologies (Wolters Kluwer Health)
