Douzinas E E, Andrianakis I, Pitaridis M T, Karmpaliotis D J, Kypriades E M, Betsou A, Gratsias Y, Sotiropoulou C, Papalois A, Roussos C
Evangelismos Hospital, Department of Critical Care, University of Athens Medical School, Greece.
Intensive Care Med. 2001 Jan;27(1):269-75. doi: 10.1007/s001340000796.
Reactive oxygen species contribute to membrane lipid peroxidation and neuronal death and have been implicated in anoxic encephalopathy. We tested whether hypoxemic reperfusion (HR) after global cerebral ischemia would improve neurological recovery.
Two groups of pigs (n = 11 in each group) were subjected to a model of a 10-min global cerebral and systemic ischemia to compare the effect of hypoxemic reperfusion (group HR) with the classical hyperoxemic control (group C). A third group not subjected to ischemia served as control to the control group (n = 6, group CC), but received hyperoxygenation at the respective period of reperfusion. The outcome was evaluated by means of neurological assessment and the extent of lipid peroxidation measuring the plasma malonaldehyde (MDA) together with hydroxyalkenals (HALK).
Animals of group HR exhibited a significantly superior neurological outcome compared with those of group C at all three consecutive assessments after reperfusion (post-resuscitation P = 0.006, at 8 h P = 0.003, and at 24 h P = 0.007). The levels of MDA and HALK are lower in the HR group than in group C (P = 0.029). Additionally, in the CC group these molecules increased significantly early at hyperoxygenation (P = 0.02). A faster lactate metabolism in the HR group was observed during reperfusion, though non-significant.
Hypoxemic reperfusion during resuscitation from a severe global ischemic cerebral insult improves the neurological outcome compared with classic hyperoxemic reperfusion. This is additionally confirmed by the decreased production of the molecules of lipid peroxidation. In the absence of preceding ischemia, these molecules may increase by simple over-oxygenation.
活性氧会导致膜脂质过氧化和神经元死亡，并且与缺氧性脑病有关。我们测试了全脑缺血后的低氧再灌注（HR）是否会改善神经功能恢复。
两组猪（每组n = 11）接受10分钟的全脑和全身缺血模型，以比较低氧再灌注组（HR组）与经典高氧对照组（C组）的效果。第三组未经历缺血，作为对照组的对照（n = 6，CC组），但在各自的再灌注期接受高氧处理。通过神经学评估以及测量血浆丙二醛（MDA）和羟基烯醛（HALK）来评估脂质过氧化程度，从而评估结果。
与C组相比，HR组动物在再灌注后的连续三次评估中均表现出明显更好的神经学结果（复苏后P = 0.006，8小时时P = 0.003，24小时时P = 0.007）。HR组中MDA和HALK的水平低于C组（P = 0.029）。此外，在CC组中，这些分子在高氧处理早期显著增加（P = 0.02）。在再灌注期间观察到HR组的乳酸代谢更快，尽管不显著。
与经典的高氧再灌注相比，严重全脑缺血性损伤复苏期间的低氧再灌注可改善神经学结果。脂质过氧化分子产生减少进一步证实了这一点。在没有先前缺血的情况下，这些分子可能会因单纯的过度氧合而增加。
