Johnson, Bruce

Background Exposure to hypoxia causes pulmonary vasoconstriction (HPV) and may contribute to the pathogenesis of HAPE. The site of HPV, however, is controversial. While the majority of data suggests HPV occurs in the pulmonary arterioles (precapillary), there is evidence that HPV may also occur in postcapillary vessels. Expansion of pulmonary capillary blood volume (Vc) is primarily passive and thus closely linked to cardiac output (Q). Purpose To examine relationships between Q and Vc during exposure to hypoxia and fluid loading. Methods/Results Healthy adults (n=25, age=31±2 yr) reported to the lab for 2 exposures: 1) 17‐h 12.5% F I O 2 in a hypoxia tent, and 2) fluid loading using IV saline (30 ml/kg over ~15 min). Q, Vc and Dm (alveolar‐capillary conductance) were measured using a rebreathe method with small amounts of C 2 H 2 , CO and NO gas. Saline infusion caused an increase in Q (32±6%, P <0.01) and Vc (39±13%, P <0.05), and a decrease in Dm (−9±3%, P <0.05). Vc/Q was not different pre‐ vs post‐saline (17±2 vs 18±3, P =0.40). Hypoxic exposure caused an increase in pulmonary arterial pressure (67±11%, P <0.01), Vc (57±20%, P =0.04) and Dm (35±6%, P <0.01) despite no change in Q (0.2±2.8%, P =0.98). Vc/Q was greater post‐ vs. pre‐hypoxia (24±4 vs. 17±2, P =0.06). Conclusion The rise in Vc with a constant Q during hypoxic exposure suggests a post capillary site for HPV causing the expansion of the pulmonary capillary bed. HL71478.