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Magnetic Resonance Imaging of Uneven Pulmonary Perfusion in Hypoxia in Humans

Sports Medicine, Internal Medicine VII; Cardiology, Internal Medicine III; Pediatric Radiology, University Hospital, Heidelberg; Departments of Radiology and Medical Physics in Radiology, German Cancer Research Center, Heidelberg; and Department of Clinical Radiology, University Medical Center Grosshadern, Ludwigs-Maximilians-University, Munich, Germany

Correspondence and requests for reprints should be addressed to Christoph Dehnert, M.D., University Hospital Heidelberg, Internal Medicine VII, Sports Medicine, Im Neuenheimer Feld 410, D-69120 Heidelberg, Germany. E-mail: christoph.dehnert{at}med.uni-heidelberg.de

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.

Key Words: high-altitude pulmonary edema • hypoxic pulmonary vasoconstriction • pulmonary artery pressure

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Uneven hypoxic pulmonary vasoconstriction (HPV) has been suggested to explain development of high-altitude pulmonary edema (HAPE). Increased inhomogeneity of HPV was found in animals and recently in a few HAPE-susceptible humans (HAPE-S) but not in control subjects using arterial spin-labeling MRI. What This Study Adds to the Field Inhomogeneity of HPV increases in hypoxia in all subjects but more in HAPE-S, suggesting that inhomogenous HPV is a more general phenomenon in animals and humans alike.

 

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