Oxygen dependency and precision of cytochrome oxidase signal from full spectral NIRS of the piglet brain
Oxygen dependency and precision of cytochrome oxidase signal from full spectral NIRS of the piglet brain
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DOI：
10.1152/ajpheart.2000.279.5.h2202
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发表时间：
2000-11-01
影响因子：
4.8
通讯作者：
Delpy, DT
中科院分区：
文献类型：
--
作者：
Springett, R;Newman, J;Delpy, DT
在短暂的缺氧波动期间，在正常碳酸血症和高碳酸血症（动脉PCO 2约为55 mmHg）的脑细胞色素氧化酶的铜A（Cu-A）中心的氧化变化进行了测量。高碳酸血症使总血红蛋白从37.5 +/- 9.1增加到50.8 +/- 12.9 μ mol/l（平均值+/- SD; n = 7），使平均脑饱和度（Smc（O2））从65 +/- 4增加到77 +/-3%，使Cu-A氧化0.43 +/- 0.23 μ mol/l。在缺氧发作期间，Cu-A氧化态没有显著变化，直到Smc（O2）分别降至43 +/- 5和21 +/- 6%（正常碳酸血症和高碳酸血症），在高碳酸血症时，缺氧时的最大降低无显著差异（1.49 +/- 0.40 μ mol/l）与正常碳酸血症（1.53 +/- 0.44 μ mol/l）相比。用于转换近红外光谱的浓度的最小二乘拟合算法的残差，并示出是小的衰减归因于铜-A信号的分量相比。从这些观察结果，我们得出结论，在这个模型中，血红蛋白和铜-A信号之间的干扰最小，铜-A氧化状态是独立的脑氧合在常氧，高碳酸血症后的氧化不是增加脑氧合的结果。
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.