Subject: Heart Failure
Author: ironjustice@aol.comDate: 4 Jul
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1797062
The autonomic nervous system at high altitude
Roger Hainsworth,1 Mark J. Drinkhill,1 and Maria Rivera-Chira2
1Institute for Cardiovascular Research, University of Leeds, Leeds,
LS2 9JT UK
2Depto. Academico Ciencias, Biologicas y Fisiologicas, UPCH, Lima,
Peru
Roger Hainsworth, Phone: +44-113/3434-821, Fax: +44-113/3434-803,
Email: r.hainsworth@leeds.ac.uk.
Corresponding author.
Received January 2, 2007; Accepted January 3, 2007.
Abstract
The effects of hypobaric hypoxia in visitors depend not only on the
actual elevation but also on the rate of ascent.
Sympathetic activity increases and there are increases in blood
pressure and heart rate.
Pulmonary vasoconstriction leads to pulmonary hypertension,
particularly during exercise.
The sympathetic excitation results from hypoxia, partly through
chemoreceptor reflexes and partly through altered baroreceptor
function.
High pulmonary arterial pressures may also cause reflex systemic
vasoconstriction.
Most permanent high altitude dwellers show excellent adaptation
although there are differences between populations in the extent of
the ventilatory drive and the erythropoiesis.
Some altitude dwellers, particularly Andeans, may develop chronic
mountain sickness, the most prominent characteristic of which being
excessive polycythaemia.
Excessive hypoxia due to peripheral chemoreceptor dysfunction has been
suggested as a cause.
The hyperviscous blood leads to pulmonary hypertension, symptoms of
cerebral hypoperfusion, and eventually right heart failure and death.
Keywords: altitude, mountain sickness, hypoxia, polycythemia,
respiration, chemoreceptors, baroreceptors, autonomic nervous system
Clin Auton Res. 2007 February; 17(1): 13–19.
Published online 2007 January 30. doi: 10.1007/s10286-006-0395-7.
PMCID: PMC1797062
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