Catecholamine Levels in Hypoxia-Induced Acute Mountain Sickness
Kamimori GH, Ryan EJ, Otterstetter R, Barkley JE, Glickman EL, Davis HQ. Catecholamine levels in hypoxia-induced acute mountain sickness. Aviat Space Environ Med 2009; 80:376–80.
Enhanced sympathoadrenal activity has been implicated in the pathogenesis of acute mountain sickness (AMS). This study was designed to examine the time course of circulating catecholamines in individuals with and without AMS. Methods: Subjects were low-altitude residents (10 men, 8 women) who had not been exposed to altitude within the previous 2 mo. They breathed 12% O2 (hypoxia equivalent to 4600 m altitude) for 8 h while seated at rest. AMS was evaluated using Lake Louise scores (LLS) at 0, 1, 3, 5, and 7 h of exposure using a threshold of 3 to define AMS. Blood samples were collected to measure arterial blood gases and oxygen saturation as well as arterial and venous epinephrine (A-EPI and V-EPI) and norepinephrine (A-NE and V-NE). Results: Eight subjects (44%) developed AMS at some time during the experiment. Blood gases showed no significant difference between subjects with or without symptoms (AMS+ and AMS−, respectively). However, AMS+ subjects showed significantly greater concentrations of A-EPI over the 8 h without any between-group difference in V-EPI. Levels of A-NE were significantly higher at baseline and during the first hour of hypoxia in subjects who later developed AMS. V-NE increased significantly over time among all participants with no difference between groups. Conclusions: These findings suggest a possible physiological marker for individuals who may be relatively susceptible to AMS and provide additional insight into the sympathoadrenal response to acute hypoxia.
Enhanced sympathoadrenal activity has been implicated in the pathogenesis of acute mountain sickness (AMS). This study was designed to examine the time course of circulating catecholamines in individuals with and without AMS. Methods: Subjects were low-altitude residents (10 men, 8 women) who had not been exposed to altitude within the previous 2 mo. They breathed 12% O2 (hypoxia equivalent to 4600 m altitude) for 8 h while seated at rest. AMS was evaluated using Lake Louise scores (LLS) at 0, 1, 3, 5, and 7 h of exposure using a threshold of 3 to define AMS. Blood samples were collected to measure arterial blood gases and oxygen saturation as well as arterial and venous epinephrine (A-EPI and V-EPI) and norepinephrine (A-NE and V-NE). Results: Eight subjects (44%) developed AMS at some time during the experiment. Blood gases showed no significant difference between subjects with or without symptoms (AMS+ and AMS−, respectively). However, AMS+ subjects showed significantly greater concentrations of A-EPI over the 8 h without any between-group difference in V-EPI. Levels of A-NE were significantly higher at baseline and during the first hour of hypoxia in subjects who later developed AMS. V-NE increased significantly over time among all participants with no difference between groups. Conclusions: These findings suggest a possible physiological marker for individuals who may be relatively susceptible to AMS and provide additional insight into the sympathoadrenal response to acute hypoxia.
Keywords: altitude sickness; epinephrine; norepinephrine
Document Type: Research Article
Publication date: 01 April 2009
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