Oxygen dependency and precision of cytochrome oxidase signal from full spectral NIRS of the piglet brain

Abstract

Oxidation changes of the copper A (CuA) center of cytochrome oxidase in the brain were measured during brief anoxic swings at both normocapnia and hypercapnia (arterial Pco 2 ≈55 mmHg). Hypercapnia increased total hemoglobin from 37.5 ± 9.1 to 50.8 ± 12.9 μmol/l (means ± SD; n = 7), increased mean cerebral saturation (SmcO2 ) from 65 ± 4 to 77 ± 3%, and oxidized CuA by 0.43 ± 0.23 μmol/l. During the onset of anoxia, there were no significant changes in the CuA oxidation state until SmcO2 had fallen to 43 ± 5 and 21 ± 6% at normocapnia and hypercapnia, respectively, and the maximum reduction during anoxia was not significantly different at hypercapnia (1.49 ± 0.40 μmol/l) compared with normocapnia (1.53 ± 0.44 μmol/l). Residuals of the least squares fitting algorithm used to convert near-infrared spectra to concentrations are presented and shown to be small compared with the component of attenuation attributed to the CuAsignal. From these observations, we conclude that there is minimal interference between the hemoglobin and CuA signals in this model, the CuA oxidation state is independent of cerebral oxygenation at normoxia, and the oxidation after hypercapnia is not the result of increased cerebral oxygenation.