Quantification of venous vessel size in human brain in response to hypercapnia and hyperoxia using magnetic resonance imaging

Authors


  • This article was published online 5 April 2012. Trevor Ahearn, Matthew Clemence, and Christian Schwarzbauer have subsequently been acknowledged as coauthors. This notice is included in the print and online versions to indicate that both have been corrected 26 April 2013.

Abstract

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 R2* and R2 that are induced by breathing 6% CO2 or pure oxygen. The experimental paradigm consisted of two 3-min intervals of inhaling 6% CO2 or 100% O2 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 R2* and R2, 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.

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