Rationale: Inhomogeneous hypoxic pulmonary vasoconstriction causing regional overperfusion and high capillary pressure is postulated for explaining how high pulmonary artery pressure leads to high-altitude pulmonary edema in susceptible (HAPE-S) individuals.
Objective: Because different species of animals also show inhomogeneous hypoxic pulmonary vasoconstriction, we hypothesized that inhomogeneity of lung perfusion in general increases in hypoxia, but is more pronounced in HAPE-S. For best temporal and spatial resolution, regional pulmonary perfusion was assessed by dynamic contrast-enhanced magnetic resonance imaging.
Methods: Dynamic contrast-enhanced magnetic resonance imaging and echocardiography were performed during normoxia and after 2 h of hypoxia (Fi(O2) = 0.12) in 11 HAPE-S individuals and 10 control subjects. As a measure for perfusion inhomogeneity, the coefficient of variation for two perfusion parameters (peak signal intensity, time-to-peak) was determined for the whole lung and isogravitational slices.
Results: There were no differences in perfusion inhomogeneity between the groups in normoxia. In hypoxia, analysis of coefficients of variation indicated a greater inhomogeneity in all subjects, which was more pronounced in HAPE-S compared with control subjects. Discrimination between HAPE-S and control subjects was best in gravity-dependent lung areas. Pulmonary artery pressure during hypoxia increased from 22 +/- 3 to 53 +/- 9 mm Hg in HAPE-S and 24 +/- 4 to 33 +/- 6 mm Hg in control subjects (mean +/- SD; p < 0.001), respectively.
Conclusion: This study shows that hypoxic pulmonary vasoconstriction is inhomogeneous in hypoxia in humans, particularly in HAPE-S individuals where it is accompanied by a greater increase in pulmonary artery pressure compared with control subjects. These findings support the hypothesis of exaggerated and uneven hypoxic pulmonary vasoconstriction in HAPE-S individuals.