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

Oxidation changes of the copper A (Cu-A) center of cytochrome oxidase in the brain were measured during brief anoxic swings at both normocapnia and hypercapnia (arterial PCO2 approximate to 55 mmHg). Hypercapnia increased total hemoglobin from 37.5 +/- 9.1 to 50.8 +/- 12.9 mu mol/l (means +/- SD; n = 7), increased mean cerebral saturation (Smc(O2)) from 65 +/- 4 to 77 +/- 3%, and oxidized Cu-A by 0.43 +/- 0.23 mu mol/l. During the onset of anoxia, there were no significant changes in the Cu-A oxidation state until Smc(O2) 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 mu mol/l) compared with normocapnia (1.53 +/- 0.44 mu mol/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 Cu-A signal. From these observations, we conclude that there is minimal interference between the hemoglobin and Cu-A signals in this model, the Cu-A oxidation state is independent of cerebral oxygenation at normoxia, and the oxidation after hypercapnia is not the result of increased cerebral oxygenation.