Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 59: 909-915, 1985;
8750-7587/85 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Reeves, J. T.
Right arrow Articles by Weil, J. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reeves, J. T.
Right arrow Articles by Weil, J. V.

Journal of Applied Physiology, Vol 59, Issue 3 909-915, Copyright © 1985 by American Physiological Society

ARTICLES

Headache at high altitude is not related to internal carotid arterial blood velocity

J. T. Reeves, L. G. Moore, R. E. McCullough, R. G. McCullough, G. Harrison, B. I. Tranmer, A. J. Micco, A. Tucker and J. V. Weil

The cause of headache in persons going to high altitude is unknown. Relatively severe hypoxemia in susceptible subjects could induce large increases in cerebral blood flow that then could initiate the headache. Thus we measured noninvasively, by Doppler ultrasound, changes in internal carotid arterial blood velocity (velocity) in 12 subjects in Denver (1,600 m) and repeatedly up to 7 h at a simulated altitude of 4,800 m (barometric pressure = 430 Torr). Six subjects, selected because of prior history of high-altitude headache, developed comparatively severe headache at 4,800 m, and four subjects, without such history, remained well. Two subjects developed moderate headache. Velocity at 4,800 m did not correlate with symptom development, arterial O2 saturation, or end-tidal PCO2. Also, neither velocity nor blood pressure was consistently elevated above the Denver base-line values. During measurements of hypercapnic ventilatory response in Denver, velocity increased linearly with end-tidal PCO2, confirming that our Doppler method could demonstrate an increase. Also, 30 min of isocapnic or poikilocapnic hypoxia caused small increases in velocity (+8 and +6%) during the base-line measurement at low altitude. Although even a small increase in cerebral perfusion could contribute to headache symptoms at high altitude, cerebral blood flow does not appear to play a primary role.


This article has been cited by other articles:


Home page
 StrokeHome page
A. Van Osta, J.-J. Moraine, C. Melot, H. Mairbaurl, M. Maggiorini, and R. Naeije
Effects of High Altitude Exposure on Cerebral Hemodynamics in Normal Subjects
Stroke, March 1, 2005; 36(3): 557 - 560.
[Abstract] [Full Text] [PDF]

Home page
 Br. J. Sports. Med.Home page
S Grant, N MacLeod, J W Kay, M Watt, S Patel, A Paterson, and A Peacock
Sea level and acute responses to hypoxia: do they predict physiological responses and acute mountain sickness at altitude?
Br. J. Sports Med., April 1, 2002; 36(2): 141 - 146.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
R. W. Baumgartner, I. Spyridopoulos, P. Bartsch, M. Maggiorini, and O. Oelz
Acute mountain sickness is not related to cerebral blood flow: a decompression chamber study
J Appl Physiol, May 1, 1999; 86(5): 1578 - 1582.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
G. F. A. Jansen, A. Krins, and B. Basnyat
Cerebral vasomotor reactivity at high altitude in humans
J Appl Physiol, February 1, 1999; 86(2): 681 - 686.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online