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

1  Department of Medical Physics and Bioengineering and 2  Department of Obstetrics, University College London, London WC1E 6JA, United Kingdom 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 hyperca...

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Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2000-11, Vol.279 (5), p.H2202-H2209
Main Authors: Springett, R, Newman, J, Cope, M, Delpy, D. T
Format: Article
Language:English
Subjects:
Animals
Blood Pressure
Brain - metabolism
Copper - analysis
Electron Transport Complex IV - metabolism
Heart Rate
Hemoglobins - analysis
Hemoglobins - metabolism
Hypercapnia - metabolism
Hypoxia, Brain - metabolism
Male
Oxidation-Reduction
Oxygen - metabolism
Oxyhemoglobins - analysis
Oxyhemoglobins - metabolism
Regression Analysis
Reproducibility of Results
Spectroscopy, Near-Infrared
Swine
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Summary:1  Department of Medical Physics and Bioengineering and 2  Department of Obstetrics, University College London, London WC1E 6JA, United Kingdom 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 P CO 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 (Smc O 2 ) from 65 ± 4 to 77 ± 3%, and oxidized Cu A by 0.43 ± 0.23   µmol/l. During the onset of anoxia, there were no significant changes in the Cu A oxidation state until Smc O 2 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 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. near-infrared spectroscopy; cytochrome oxidase; hypercapnia
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2000.279.5.h2202