灵长类动物革兰氏阴性感染性休克时线粒体氧化还原反应的改变。

Circulatory shock Pub Date : 1994-05-01
S G Simonson, K Welty-Wolf, Y T Huang, J A Griebel, M S Caplan, P J Fracica, C A Piantadosi
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引用次数: 0

摘要

革兰氏阴性败血症引起氧供需关系的改变。我们使用了一种由静脉输注大肠杆菌(E. coli)产生的高动力革兰氏阴性脓毒症灵长类动物模型来评估脓毒症诱导的线粒体氧化还原(氧化还原)状态在体内肌肉中的改变。采用近红外(NIR)光谱法测定了完整前臂线粒体内呼吸链末端细胞色素a,a3的氧化还原状态。将肌肉近红外数据与常规的氧输送(DO2)和耗氧量(VO2)进行比较。在大肠杆菌输注和液体复苏后,DO2和VO2在24小时的脓毒症中变化很小。相比之下,近红外评价的细胞色素a,a3氧化还原状态的变化发生在几小时内,并且是进行性的。线粒体功能反应与连续肌肉活检观察到的结构变化相关。一些动物早在12小时就出现了肌肉线粒体的大体形态变化,大多数动物在24小时就出现了。近红外光谱显示,形态学变化与氧化能力下降一致。近红外数据还表明,有两种机制可以解释致死性败血症中氧代谢和线粒体功能的异常。这些机制包括线粒体供氧的早期缺陷,随后是肌肉中功能性细胞色素a,a3的逐渐丧失。
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Altered mitochondrial redox responses in gram negative septic shock in primates.

Gram negative sepsis causes changes in oxygen supply-demand relationships. We have used a primate model of hyperdynamic gram negative sepsis produced by intravenous infusion of Escherichia coli (E. coli) to evaluate sepsis-induced alterations in mitochondrial oxidation-reduction (redox) state in muscle in vivo. The redox state of cytochrome a,a3, the terminal member of the intramitochondrial respiratory chain, was assessed in the intact forearm by near-infrared (NIR) spectroscopy. The muscle NIR data were compared to routine measures of oxygen delivery (DO2) and oxygen consumption (VO2). After E. coli infusion and fluid resuscitation, DO2 and VO2 showed minimal changes through 24 hr of sepsis. In contrast, changes in cytochrome a,a3 redox state evaluated by NIR occurred within a few hours and were progressive. Mitochondrial functional responses were correlated with structural changes observed on serial muscle biopsies. Gross morphological changes in muscle mitochondria were present in some animals as early as 12 hr, and, in most animals, by 24 hr. The morphologic changes were consistent with decreases in oxidative capacity as suggested by NIR spectroscopy. The NIR data also suggest that two mechanisms are operating to explain abnormalities in oxygen metabolism and mitochondrial function in lethal sepsis. These mechanisms include an early defect in oxygen provision to mitochondria that is followed by a progressive loss in functional cytochrome a,a3 in the muscle.

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