Wiernsperger N, Gygax P
Adv Exp Med Biol. 1983;159:5-15. doi: 10.1007/978-1-4684-7790-0_2.
Cerebral blood volume, hemoglobin saturation and the cytochrome a, a3 redox state were monitored simultaneously by using three wavelengths of light in the near infrared portion of the spectrum for transillumination of the intact skull of rats. The changes in these parameters following incomplete cerebral ischemia were assessed in Wistar and Long-Evans rats submitted to carotid ligation. Another group of Wistar rats was submitted to vertebral + carotid occlusion. The experiments, performed under N2O/O2 anesthesia, showed that in all three groups carotid occlusion induced a decrease in blood volume, Hb saturation and a reduction of cyt. a, a3. However, the cytochrome redox state tended to normalize during ischemia as a consequence of higher O2 extraction from blood. The primary finding of this study was the marked hyperoxidation of cyt. a, a3 which occurred after reestablishing of the carotid blood supply, in spite of a secondary post-ischemic hypoperfusion of the brain. Although uncoupling of oxidative phosphorylation cannot be excluded the dissociation between blood supply and metabolism could well be due to ischemia-induced hypermetabolism of the central nervous tissue. In view of the marked oxidation of cyt. a, a3 during the reperfusion period as compared with the small extent of its reduction during the ischemic episode, the data also support the hypothesis that under steady state conditions in vivo, cytochrome oxidase is mainly reduced.
利用光谱近红外部分的三个波长对大鼠完整颅骨进行透照,同时监测脑血容量、血红蛋白饱和度和细胞色素a、a3的氧化还原状态。在接受颈动脉结扎的Wistar和Long-Evans大鼠中评估不完全脑缺血后这些参数的变化。另一组Wistar大鼠接受椎动脉+颈动脉闭塞。在N2O/O2麻醉下进行的实验表明,在所有三组中,颈动脉闭塞均导致血容量、血红蛋白饱和度降低以及细胞色素a、a3减少。然而,由于从血液中提取更多的氧气,细胞色素氧化还原状态在缺血期间趋于正常化。本研究的主要发现是,尽管脑缺血后存在继发性灌注不足,但在恢复颈动脉血液供应后,细胞色素a、a3出现明显的过氧化。虽然不能排除氧化磷酸化解偶联,但血液供应与代谢之间的解离很可能是由于缺血诱导的中枢神经组织代谢亢进。鉴于再灌注期细胞色素a、a3的氧化程度明显高于缺血期其还原程度,这些数据也支持以下假设:在体内稳态条件下,细胞色素氧化酶主要处于还原状态。