Acute high-altitude exposure reduces lung diffusion: data from the HIGHCARE Alps project

Area of Science:

• High-altitude physiology
• Pulmonary medicine
• Respiratory system research

Background:

• The mechanisms of lung fluid accumulation and alveolar-capillary membrane integrity at high altitudes remain unclear.
• Acute high-altitude exposure may lead to pulmonary edema and compromise gas exchange efficiency.

Purpose of the Study:

• To investigate the development of lung fluid and alveolar-capillary membrane damage during acute high-altitude exposure.
• To assess the impact of high altitude on lung carbon monoxide diffusion (DLCO) and its components.

Main Methods:

• Healthy subjects (n=43) underwent measurements of DLCO, membrane diffusion (DM), capillary volume (VC), and alveolar volume (VA) at low altitude and after 1 and 3 days at high altitude (4559 m).
• Plasma surfactant protein B (SPB) and Receptor of Advanced Glycation End-products (RAGE) were measured as markers of alveolar-capillary membrane damage.
• Ultrasound lung comets were used to quantify extravascular lung water; acetazolamide or placebo was administered to assess its effect.

Main Results:

• DLCO decreased significantly at high altitude due to a reduction in DM, partially offset by an increase in VC.
• Ultrasound lung comets increased significantly, indicating elevated extravascular lung water, irrespective of acetazolamide treatment.
• Plasma SPB and RAGE levels remained unchanged, suggesting that plasma markers did not reflect the observed lung fluid changes.

Conclusions:

• Acute high-altitude exposure leads to increased lung fluid accumulation, evidenced by ultrasound lung comets.
• The observed reduction in DLCO, driven by DM decrease, coupled with increased lung water, supports the hypothesis of alveolar-capillary membrane compromise.
• Plasma-based markers (SPB, RAGE) may not be sensitive indicators of high-altitude-induced alveolar-capillary membrane stress.