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.
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.
Authors: Michael D Patz; Rui C Sá; Chantal Darquenne; Ann R Elliott; Amran K Asadi; Rebecca J Theilmann; David J Dubowitz; Erik R Swenson; G Kim Prisk; Susan R Hopkins Journal: J Appl Physiol (1985) Date: 2017-01-05
Authors: Jochen Kressler; Mark Stoutenberg; Bernard A Roos; Anne L Friedlander; Arlette C Perry; Joseph F Signorile; Kevin A Jacobs Journal: Eur J Appl Physiol Date: 2011-03-31 Impact factor: 3.078
Authors: T J Arai; A C Henderson; D J Dubowitz; D L Levin; P J Friedman; R B Buxton; G K Prisk; S R Hopkins Journal: J Appl Physiol (1985) Date: 2008-12-04
Authors: Shelley X L Zhang; James J Miller; Donna Beer Stolz; Laura D Serpero; Wei Zhao; David Gozal; Yang Wang Journal: Am J Respir Cell Mol Biol Date: 2008-09-05 Impact factor: 6.914