Post-cardiac arrest hyperoxia and mitochondrial function.
Post-cardiac arrest hyperoxia and mitochondrial function.
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DOI：
10.1016/s0300-9572(11)70151-4
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发表时间：
2011-12-01
期刊：
影响因子：
6.5
通讯作者：
Aune, Sverre E
中科院分区：
文献类型：
--
作者：
Angelos, Mark G;Yeh, Steve T;Aune, Sverre E
简介：缺血后快速复氧是使缺血损伤最小化所必需的，但其本身可通过诱导活性氧而引起进一步的再灌注损伤。细胞内氧的利用主要发生在线粒体中。本研究的目的是确定心脏停搏和自主循环恢复（ROSC）后1小时控制动脉氧合后心脏线粒体功能。我们推测，动脉氧合过度ROSC后会导致心脏线粒体功能的更大的损害。心脏骤停6.5分钟后，用标准thumper CPR、通气和肾上腺素复苏动物。在ROSC之后，所有动物都用100%O（2）或40%O（2）滴定通气60分钟，以利用脉搏血氧仪达到正常氧。结果：ROSC后100%O2组动脉PaO 2为280 ± 40，40%O2组为105 ± 10; ROSC后1小时，100%O（2）通气的动物心脏线粒体状态3呼吸和呼吸控制比（状态3/4呼吸）较基线显著降低，但40%O（2）通气的动物则无此变化。结论：短暂心脏骤停后ROSC后动脉高氧加重线粒体功能受损。这些发现的总体临床意义尚不清楚，需要更多的工作来更好地了解停搏后高氧对心脏和线粒体功能的作用。
INTRODUCTION: Rapid post-ischemic re-oxygenation is necessary to minimize ischemic injury, but itself can induce further reperfusion injury through the induction of reactive oxygen species. Utilization of oxygen within the cell primarily occurs in the mitochondria. The objective of this study was to determine heart mitochondrial function after 1 h of controlled arterial oxygenation following cardiac arrest and restoration of spontaneous circulation (ROSC). We hypothesized that arterial hyper-oxygenation following ROSC would result in greater impairment of heart mitochondrial function.METHODS: KCl cardiac arrest was induced in anesthetized rats. Following 6.5 min of cardiac arrest, animals were resuscitated with standard thumper CPR, ventilation and epinephrine. Following ROSC, all animals were ventilated for 60 min with either 100% O(2) or 40% O(2) titrated to achieve normoxia utilizing pulse oximetry. At the end of 1 h, heart mitochondria were isolated and mitochondrial respiratory function was measured.RESULTS: Post-ROSC arterial PaO2 was 280 ± 40 in the 100% O2 group and 105 ± 10 in the 40% O2 group. One hour after ROSC, heart mitochondrial state 3 respirations and respiration control ratio (state 3/4 respiration) were significantly reduced from baseline in animals ventilated with 100% O(2), but not with 40% O(2).CONCLUSION: Post-ROSC arterial hyperoxia after a short cardiac arrest exacerbates impaired mitochondrial function. The overall clinical significance of these findings is unclear and requires additional work to better understand the role of post-arrest hyperoxia on cardiac and mitochondrial function.