K.A. Shah1, K. DiMarco1, K.M. Beasley1, J.P. Speros1, J.E. Elliott2,3, S.S. Laurie4,J.W. Duke5, R.D. Goodman6, E. Futral6, J.A. Hawn6, R.C. Roach7, A.T. Lovering1

1University of Oregon, Eugene, OR, USA; 2VA Portland Health Care System, Portland, OR, USA; 3Oregon Health and Science University, Portland, OR, USA; 4 NASA Johnson Space Center, Houston, TX, USA; 5 Northern Arizona University, Flagstaff, AZ, USA; 6 Oregon Heart and Vascular Institute, Springfield, OR, USA; 7 University of Colorado Anschutz Medical Campus, Aurora, CO, USA

Acute mountain sickness (AMS) occurs when individuals rapidly ascend to high altitudes, but its exact cause remains unknown. Additionally, AMS is assessed using a subjective questionnaire with a variety of criteria used for diagnosis so there is no precise, objective method for determining if a subject has AMS. Hypoxia, or low oxygen, at altitude results in a proinflammatory state and AMS is associated with systemic inflammation as determined by elevated plasma levels of some cytokines. PURPOSE: To determine if the association between AMS and inflammation was altered based on how AMS was defined. METHODS: 17 women and 17 men were exposed to 10 hours of normobaric hypoxia (11.5% O2) simulating 15600 feet. Blood samples taken before and at 10 hours of hypoxia were assayed for 13 inflammatory cytokines. AMS was defined by the following definitions: 1) Lake Louise Questionnaire (LLQ) score ³3 and a headache score ³1 at the 10-hour time point, 2) maximum LLQ score ³3 and a maximum headache score of ³1, 3) maximum LLQ score ³3 and a maximum Environmental Symptoms Questionnaire (ESQ) score of 0.7 or maximum LLQ ³3, a maximum headache score ³2, and a maximum ESQ ³0.4, 4) maximum LLQ ³3, 5) LLQ score ³3 at the 10-hour time point. RESULTS: We found that Interleukin (IL) 8 significantly increased in AMS- but not AMS+ participants regardless of AMS definition. Additionally, AMS- but not AMS+ participants significantly increased IL-1b and IL-33 concentration from baseline to 10 hours of hypoxia under only three out of the five definitions (#1, #3 & #5 above for IL-1b and #3, #4, & #5 above for IL-33). Furthermore, the change in IL-1b concentration after 10 hours of hypoxia was significantly different between AMS- and AMS+ participants under definition #3 above. CONCLUSION: These data suggest that how AMS is defined may influence whether or not there are differences in circulating inflammatory cytokines between those with and without AMS. Therefore, the relationship between systemic inflammation and AMS may be more complex than previously thought.

Supported by Defense Medical Research & Development Program, DoD W81XWH-10-2-0114

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