Evidence that hypoxia‐induced pulmonary vasoconstriction in humans is primarily a post‐capillary event

Abstract

BackgroundExposure 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).PurposeTo examine relationships between Q and Vc during exposure to hypoxia and fluid loading.Methods/ResultsHealthy adults (n=25, age=31±2 yr) reported to the lab for 2 exposures: 1) 17‐h 12.5% FIO2 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 C2H2, 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).ConclusionThe 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.