The Effect of Hypercapnia on Cortical Metabolic Rate and Mitochondrial Redox Status.

Abstract

Hypercapnia is commonly used as a vasodilatory stimulus in both basic and clinical research. There have been conflicting reports about whether cerebral metabolic rate of oxygen (CMRO2) is maintained at normal levels during increases of cerebral blood flow (CBF) and oxygen delivery caused by hypercapnia.This study aims to provide insight into how hypercapnia may impact CMRO2 and brain mitochondrial function. We introduce data from mouse cortex collected with a novel multimodality system which combines MRI and near-infrared spectroscopy (NIRS). We quantify CBF, tissue oxygen saturation (StO2), oxidation state of the mitochondrial enzyme cytochrome c oxidase (CCO), and CMRO2.During hypercapnia, CMRO2 did not change while CBF, StO2, and the oxidation state of CCO increased significantly. This paper supports the conclusion that hypercapnia does not change CMRO2. It also introduces the application of a multimodal NIRS-MRI system which enables non-invasive quantification of CMRO2, and other physiological variables, in the cerebral cortex of mouse models.