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Quantification of venous vessel size in human brain in response to hypercapnia and hyperoxia using magnetic resonance imaging
Author(s) -
Shen Yuji,
Pu Ida M.,
Ahearn Trevor,
Clemence Matthew,
Schwarzbauer Christian
Publication year - 2013
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.24258
Subject(s) - hyperoxia , hypercapnia , white matter , vasodilation , vasoconstriction , anesthesia , chemistry , medicine , magnetic resonance imaging , lung , acidosis , radiology
Hypercapnia and hyperoxia give rise to vasodilation and vasoconstriction, respectively. This study investigates the influence of hypercapnia and hyperoxia on venous vessel size in the human brain. Venous vessel radii were measured in response to hypercapnia and hyperoxia. The venous vessel radii were determined by calculation of the changes in R 2 * and R 2 that are induced by breathing 6% CO 2 or pure oxygen. The experimental paradigm consisted of two 3‐min intervals of inhaling 6% CO 2 or 100% O 2 interleaved with three 2‐min intervals of breathing air. Hypercapnic and hyperoxic experiments were performed on eight subjects on a 3T scanner. Parametric maps of mean venous vessel radius were calculated from the changes in R 2 * and R 2 , which were measured by simultaneous acquisition of gradient‐echo and spin‐echo signals. The mean venous vessel radii in hypercapnia were 7.3 ± 0.3 μm in gray matter and 6.6 ± 0.5 μm in white matter. The corresponding vessel radii in hyperoxia were 5.6 ± 0.2 μm in gray matter and 5.4 ± 0.2 μm in white matter. These results show that the venous vessel radius was larger in hypercapnia than that in hyperoxia in both gray matter and white matter ( P < 0.005), which agrees with the hypothesis that hypercapnia causes vasodilation and hyperoxia induces vasoconstriction. Magn Reson Med, 2013. © 2012 Wiley Periodicals, Inc.