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J Appl Physiol (October 31, 2003). doi:10.1152/japplphysiol.00704.2003
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Submitted on July 8, 2003
Accepted on October 27, 2003

Pathophysiological significance of peroxidative stress, neuronal damage and membrane permeability in acute mountain sickness

Damian M Bailey1*, Gian-Reto Kleger2, Manfred Holzgraefe3, Peter E Ballmer4, and Peter Bartsch5

1 Department of Physiology, University of Glamorgan, Pontypridd, South Wales, United Kingdom
2 Departments of Medicine and Radiology, University of Bern, Inselspital, Bern, Switzerland
3 Clinic for Neurological Rehabilitation, Schildautal, Seesen, Germany
4 Department of Medicine, Kantonsspital, Winterthur, Switzerland
5 Department of Sports Medicine, University of Heidelberg, Heidelberg, Germany

* To whom correspondence should be addressed. E-mail: dbailey1{at}glam.ac.uk.

Free radical-mediated changes in vascular permeability and subsequent inflammatory response may be a contributory pathogenetic cofactor responsible for the development of neurological sequelae associated with acute mountain sickness (AMS). To investigate this, forty nine subjects were examined at sea-level and serially following rapid ascent to 4,559m. While the venous concentration of total creatine phosphokinase (CPK) activity was measured in all subjects, a complimentary examination of lipid peroxidation (F2-isoprostanes), inflammatory (TNF-{alpha}, IL-1{beta}, IL-2, IL-6, IL-8, CRP) and cerebrovascular tissue damage [neuron specific enolase (NSE)] biomarkers was confined to a subcohort of twenty four subjects. A selective increase (P < 0.05) in total CPK was observed in subjects diagnozed with AMS at high-altitude (n = 25) compared to apparently healthy controls (n = 24). However, despite a marked increase in IL-6 and CRP due primarily to high-altitude pulmonary edema (HAPE), subcohort analyzes demonstrated no selective differences in F2-isoprostanes, NSE or remaining pro-inflammatory cytokines due to AMS (n = 14). The present findings are the first to demonstrate that free radical-mediated neuronal damage of sufficient degree to be detected in the peripheral circulation, does not occur and is therefore unlikely to be an important, initiating event, critical for the development of AMS. The pathophysiological significance of increased sarcolemmal membrane permeability and inflammatory response, either as a cause or epiphenomenon of AMS and/or HAPE, remains to be elucidated.




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