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Christoph Wenisch, MD; Bernie Parschalk, MD; Sonja Reichmann, MTA; Wolfgang Graninger, MD, PhD
Vienna, Austria

Christian Gruber, MD
Badgastein, Austria

Arch Intern Med. 1995;155(18):2012-2013.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Pathophysiologic mechanisms leading to high-altitude pulmonary or cerebral edema include exposure to hypobaric hypoxia, physical exhaustion, and exposure to cold.¹ After intense eccentric exercise (eg, hill running), increased levels of cytokines have been demonstrated.² We serially determined the serum levels of inflammatory cytokines and acute-phase reactants in six well-built Austrian mountaineers (aged 30 to 58 years) on their way up to Mount Manaslu in Nepal (summit, 8156 m).

All were lifelong low-altitude residents, and none had experienced any prolonged exposure to altitudes greater than 1500 m in the 6 months before the study. The findings of physical examination, medical history, ergometry, echocardiography, electrocardiography, spirometry, and routine laboratory examinations (ie, total blood cell count, blood sedimentation rate, and liver and renal function tests) were normal before the climb. All subjects gave informed consent.

Venipuncture was performed in Salzburg, Austria, before departure (baseline rest level, 300 m; no physical activity), . . . [Full Text PDF of this Article]

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