Cat brain cytochrome-c oxidase redox changes induced by hypoxia after blood-fluorocarbon exchange transfusion.

Cat brain cytochrome-c oxidase redox changes induced by hypoxia after blood-fluorocarbon exchange transfusion.
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氟碳换血后缺氧引起的猫脑细胞色素c氧化酶氧化还原变化。

DOI:
10.1152/ajpheart.1995.269.2.h417
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发表时间:
1995
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Hanley,DF
Hanley,DF
中科院分区:
--
文献类型:
--
作者:
Ferrari,M;Williams,MA;Wilson,DA;Thakor,NV;Traystman,RJ;Hanley,DF

文献摘要

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采用快速扫描近红外光谱(730-960 nm)技术,结合体感诱发电位(SEP)监测,研究了不同程度缺氧和急性缺氧对全氟代烃交换血猫脑细胞色素c氧化酶(cyt aa 3)氧化还原状态的影响。在分级缺氧[10分钟,分别在分数吸入O2浓度(FIO 2)0.9,0.8,0.7,0.6,和0.5],细胞色素aa 3减少发生在FIO 2 0.6时,脑O2输送< 3.5 ml.100 g-1.min-1。在急性缺氧(FIO 2 0.6持续10分钟)中,从5到10分钟发生显著的细胞色素aa 3减少(脑氧输送3.1 +/- 0.3 ml.100 g-1.min-1),并在复氧后恢复(FIO 2 1.0)。细胞色素aa 3氧化还原的变化之前或同时与SEP的改变在两个缺氧协议。这些结果表明,脑细胞色素aa 3的减少与严重减少的脑O2输送,但没有显着的变化,脑细胞色素aa 3氧化还原状态发生与脑O2输送的小减少。我们的结论是,脑细胞色素aa 3的实质性变化不会发生在生理水平的O2输送,目前的近红外临床仪器将检测氧依赖性脑细胞色素aa 3氧化还原变化,只有当O2输送是非常妥协。
We used rapid-scanning near-infrared (NIR) spectroscopy (730-960 nm) to study the effects of graded or acute hypoxia on cerebral cytochrome-c oxidase (cyt aa3) redox state in blood-perfluoro-carbon-exchanged cats with somatosensory evoked potential (SEP) monitoring. In graded hypoxia [10 min each at fractional inspiratory O2 concentration (FIO2) 0.9, 0.8, 0.7, 0.6, and 0.5], cyt aa3 reduction occurred at FIO2 0.6 when cerebral O2 delivery was < 3.5 ml.100 g-1.min-1. In acute hypoxia (FIO2 0.6 for 10 min), significant cyt aa3 reduction occurred from 5 to 10 min (cerebral O2 delivery 3.1 +/- 0.3 ml.100 g-1.min-1) and recovered with reoxygenation (FIO2 1.0). Cyt aa3 redox changes preceded or coincided with SEP alterations in both hypoxia protocols. These results demonstrate that cerebral cyt aa3 reduction occurs with severe reduction of cerebral O2 delivery, but no significant change in cerebral cyt aa3 redox state occurs with small reductions of cerebral O2 delivery. We conclude that substantial changes in cerebral cyt aa3 do not occur at physiological levels of O2 delivery and that current NIR clinical instruments would detect oxygen-dependent cerebral cyt aa3 redox changes only when O2 delivery is extremely compromised.