Air blood barrier phenotype correlates with alveolo-capillary O2 equilibration in hypobaric hypoxia.

The O 2 diffusion limitation across the air blood barrier (DO 2 and subcomponents Dm and Vc ) was evaluated in 17 healthy participants exposed to hypobaric hypoxia (HA, 3840m, P I O 2 ∼90 mmHg). A 10% decrease in alveolar volume ( VA ) in all participants suggested the development of sub-clinical interstitial lung edema. In >80% of participants DO 2 /VA increased, reflecting an individual strategy to cope with the hypoxia stimulus by remodulating Vc or Dm . Opposite changes in Dm / Vc ratio were observed and participants decreasing Vc showed reduced alveolar blood capillary transit time. The interplay between diffusion and perfusion (cardiac output) was estimated in order to investigate the individual adaptive response to hypoxia. It appears remarkable that despite individual differences in the adaptive response to HA, diffusion limitation did not exceed ∼11% of the alveolar-venous PO 2 gradient, revealing an admirable functional design of the air-blood barrier to defend the O 2 diffusion/perfusion function when facing hypobaric hypoxia corresponding to 50 mmHg decreased P A O 2 . [ABSTRACT FROM AUTHOR]