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Published ahead of print on August 31, 2006, doi:10.1164/rccm.200606-780OC

Am. J. Respir. Crit. Care Med., Volume 174, Number 10, November 2006, 1132-1138

A more recent version of this article appeared on November 15, 2006
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Submitted on June 13, 2006
Accepted on August 31, 2006

Magnetic Resonance Imaging of Uneven Pulmonary Perfusion in Hypoxia in Humans

Christoph Dehnert1*, Frank Risse2, Sebastian Ley3, Tristan A Kuder4, Ralf Buhmann4, Michael Puderbach4, Elmar Menold1, Derliz Mereles5, Hans-Ulrich Kauczor4, Peter Bartsch1, and Christian Fink6

1 Internal Medicine VII, Sports Medicine, University Hospital, Heidelberg, Germany, 2 Department of Medical Physics in Radiology, German Cancer Research Center, Heidelberg, Germany, 3 Department of Radiology, German Cancer Research Center, Heidelberg, Germany; Pediatric Radiology, University Hospital, Heidelberg, Germany, 4 Department of Radiology, German Cancer Research Center, Heidelberg, Germany, 5 Internal Medicine III, Cardiology, University Hospital, Heidelberg, Germany, 6 Department of Radiology, German Cancer Research Center, Heidelberg, Germany; Department of Clinical Radiology, University Medical Center Grosshadern, Ludwigs-Maximilians-University, Munich, Germany

* To whom correspondence should be addressed. 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 individuals (HAPE-S). Objective: Since different species of animals also show inhomogeneous hypoxic pulmonary vasoconstriction, we hypothesized that inhomogeneity of lung perfusion in general increases in hypoxia, but 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 hours of hypoxia (FIO2=0.12) in 11 HAPE-S and 10 controls. 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 to controls. Discrimination between HAPE-S and controls was best in gravity dependent lung areas. Pulmonary artery pressure during hypoxia increased from 22±3 to 53±9 mmHg in HAPE-S and 24±4 to 33±6 mmHg in controls (mean±SD, p<0.001), respectively. Conclusion: This study shows that hypoxic pulmonary vasoconstriction is inhomogeneous in hypoxia in humans, particularly in HAPE-S where it is accompanied by a greater increase in pulmonary artery pressure compared to controls. These findings support the hypothesis of exaggerated and uneven hypoxic pulmonary vasoconstriction in HAPE-S.
Key words: high altitude pulmonary edema, hypoxic pulmonary vasoconstriction, pulmonary artery pressure




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