ROLE OF CIRCULATING INFLAMMATION IN REGULATING PULMONARY PRESSURE AT ALTITUDE
K.G. DiMarco1, K.M. Beasley1, K. Shah1, J.P. Speros1, J.E. Elliott2,3, S.S. Laurie4, J.W. Duke5, R.D. Goodman6, E. Futral6, J.A. Hawn6, B. Hetrick1, C. McCurdy1, R.C. Roach7 and A.T. Lovering1
1University of Oregon, 2VA Portland Health Care System, 3Oregon Health and Science University, 4NASA Johnson Space Center, 5Northern Arizona University, 6Oregon Heart and Vascular Institute, 7University of Colorado Anschutz Medical Campus
A patent foramen ovale (PFO) is a right-to-left shunt present in ~30% of the population that has been shown to worsen the degree of hypoxemia at sea level, and hypoxia is a known inflammatory stimulus. At altitude, the alveolar hypoxia results in increased pulmonary pressures, but it is unknown if this effect is more pronounced in those with a PFO, or if inflammation plays a role in regulating pulmonary pressures. PURPOSE: to determine whether changes in circulating inflammation correlate with changes in pulmonary pressures during 10 hours of normobaric hypoxia and determine whether those changes are different in those with a PFO. METHODS: 36 participants matched for biological sex (18 female) and presence/absence of a PFO (18 PFO+) were exposed to 10 hours of normobaric hypoxia (11.5% O2). Venous blood samples were taken at 0 and 10 hours, and plasma was later analyzed via flow cytometry for the presence of 1 anti- and 12 pro-inflammatory cytokines. Pulmonary artery systolic pressure (PASP) and cardiac output (Q) were measured via echocardiography at 0, 4, 7, and 10 hours. Total pulmonary resistance (TPR) was calculated as PASP/Q. RESULTS: PASP (p < 0.0001), Q (p < 0.0001), and TPR (p = 0.0002) all significantly increased from baseline to 10 hours but plateaued at 7 hours. There were no differences in PASP, Q, or TPR between PFO- and PFO+ participants. The absolute change in each cytokine individually did not correlate with the absolute change in PASP. However, in a multiple linear regression model using the cytokines IL-18, IL-23, and IL-33, the change in IL-18 (p = 0.0021), IL-23 (p = 0.0031), and IL-33 (p = 0.0492) significantly predicted the change in PASP (significance of overall model, p = 0.0071). CONCLUSION: Our findings indicate that there are no effects of PFO on pulmonary pressures in response to 10 hrs of normobaric hypoxia. However, there is a positive association between the change in inflammation and the change in PASP during hypoxia exposure. These data suggest that individuals with highest levels of circulating inflammation may have an increased risk of developing higher pulmonary pressures under hypoxic conditions.
This research was supported by the Defense Medical Research & Development Program, Department of Defense; Eugene & Clarissa Evonuk Memorial Graduate Fellowship in Environmental, Exercise, or Stress Physiology.
DiMarco, KG; Beasley, KM; Shah, K; Speros, JP; Elliott, JE; Laurie, SS; Duke, JW; Goodman, RD; Futral, E; Hawn, JA; Hetrick, B; McCurdy, C; Roach, RC; and Lovering, AT
"ROLE OF CIRCULATING INFLAMMATION IN REGULATING PULMONARY PRESSURE AT ALTITUDE,"
International Journal of Exercise Science: Conference Proceedings: Vol. 8:
9, Article 24.
Available at: https://digitalcommons.wku.edu/ijesab/vol8/iss9/24