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

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 (S_tO₂), oxidation state of the mitochondrial enzyme cytochrome c oxidase (CCO), and CMRO₂.During hypercapnia, CMRO₂ did not change while CBF, S_tO₂, 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.