Hoshi Y, Hazeki O, Kakihana Y, Tamura M
Biophysics Group, Research Institute for Electronic Science, Hokkaido University, Sapporo 060, Japan.
J Appl Physiol (1985). 1997 Dec;83(6):1842-8. doi: 10.1152/jappl.1997.83.6.1842.
Using near-infrared spectroscopy, we developed a new approach for measuring the redox state of cytochrome oxidase in the brain under normal blood-circulation conditions. Our algorithm does not require the absorption coefficient of cytochrome oxidase, which differs from study to study. We employed this method for evaluation of effects of changes in oxygen delivery on cerebral oxygenation in rats. When fractional inspired oxygen was decreased in a stepwise manner from 100 to <10%, at which point the concentration of oxygenated hemoglobin ([HbO2]) decreased by approximately 60%, cytochrome oxidase started to be reduced. Increases in arterial PO2 under hyperoxic conditions caused an increase in [HbO2], whereas further oxidation of cytochrome oxidase was not observed. The dissociation of the responses of hemogloblin and cytochrome oxidase was also clearly observed after the injection of epinephrine under severely hypoxic conditions; that is, cytochrome oxidase was reoxidized with increasing blood pressure, whereas hemoglobin oxygenation was not changed. These data indicated that oxygen-dependent redox changes in cytochrome oxidase occur only when oxygen delivery is extremely impaired. This is consistent with the in vitro data of our previous study.
利用近红外光谱技术，我们开发了一种在正常血液循环条件下测量大脑中细胞色素氧化酶氧化还原状态的新方法。我们的算法不需要细胞色素氧化酶的吸收系数，而不同研究中的吸收系数有所不同。我们采用这种方法评估了氧气输送变化对大鼠脑氧合的影响。当吸入氧分数从100%逐步降至<10%时，此时氧合血红蛋白（[HbO2]）浓度降低了约60%，细胞色素氧化酶开始被还原。在高氧条件下动脉血氧分压升高导致[HbO2]增加，而未观察到细胞色素氧化酶的进一步氧化。在严重缺氧条件下注射肾上腺素后，也清楚地观察到血红蛋白和细胞色素氧化酶反应的解离；也就是说，细胞色素氧化酶随着血压升高而重新氧化，而血红蛋白氧合没有变化。这些数据表明，只有当氧气输送极度受损时，细胞色素氧化酶中才会发生依赖氧气的氧化还原变化。这与我们之前研究的体外数据一致。
