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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Normoxic resuscitation after cardiac arrest protects against hippocampal oxidative stress, metabolic dysfunction, and neuronal death.
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Normoxic resuscitation after cardiac arrest protects against hippocampal oxidative stress, metabolic dysfunction, and neuronal death.

机译：心脏骤停后进行常氧复苏可防止海马氧化应激，代谢功能障碍和神经元死亡。

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摘要

Resuscitation and prolonged ventilation using 100% oxygen after cardiac arrest is standard clinical practice despite evidence from animal models indicating that neurologic outcome is improved using normoxic compared with hyperoxic resuscitation. This study tested the hypothesis that normoxic ventilation during the first hour after cardiac arrest in dogs protects against prelethal oxidative stress to proteins, loss of the critical metabolic enzyme pyruvate dehydrogenase complex (PDHC), and minimizes subsequent neuronal death in the hippocampus. Anesthetized beagles underwent 10 mins ventricular fibrillation cardiac arrest, followed by defibrillation and ventilation with either 21% or 100% O2. At 1 h after resuscitation, the ventilator was adjusted to maintain normal blood gas levels in both groups. Brains were perfusion-fixed at 2 h reperfusion and used for immunohistochemical measurements of hippocampal nitrotyrosine, a product of protein oxidation, and the E1alpha subunit of PDHC. In hyperoxic dogs, PDHC immunostaining diminished by approximately 90% compared with sham-operated dogs, while staining in normoxic animals was not significantly different from nonischemic dogs. Protein nitration in the hippocampal neurons of hyperoxic animals was 2-3 times greater than either sham-operated or normoxic resuscitated animals at 2 h reperfusion. Stereologic quantification of neuronal death at 24 h reperfusion showed a 40% reduction using normoxic compared with hyperoxic resuscitation. These results indicate that postischemic hyperoxic ventilation promotes oxidative stress that exacerbates prelethal loss of pyruvate dehydrogenase and delayed hippocampal neuronal cell death. Moreover, these findings indicate the need for clinical trials comparing the effects of different ventilatory oxygen levels on neurologic outcome after cardiac arrest.
机译：尽管动物模型的证据表明，与高氧复苏相比，使用常氧可以改善神经系统的预后，但心脏骤停后复苏和长时间使用100％氧气进行通气是标准的临床实践。这项研究检验了以下假设：狗在心脏骤停后的第一个小时内进行的有氧通气可以防止蛋白质产生致命性的氧化应激，关键的代谢酶丙酮酸脱氢酶复合物（PDHC）的丢失，并最大程度地减少海马体随后的神经元死亡。麻醉的小猎犬心室骤停10分钟，然后用21％或100％O2除颤和通气。复苏后1小时，调整呼吸机以维持两组的正常血气水平。在再灌注2小时后将大脑灌注固定，并用于海马硝基酪氨酸（一种蛋白质氧化产物和PDHC的E1alpha亚基）的免疫组织化学测量。在高氧犬中，与假手术犬相比，PDHC免疫染色减少了约90％，而在常氧动物中的染色与非缺血犬相比没有显着差异。高氧动物海马神经元的蛋白质硝化作用在2 h再灌注时比假手术或常氧复苏动物高2-3倍。与高氧复苏相比，常氧再灌注后24小时对神经元死亡的体视学定量显示减少了40％。这些结果表明，缺血后高氧通气促进了氧化应激，加剧了丙酮酸脱氢酶的致死前损失并延迟了海马神经元细胞死亡。此外，这些发现表明需要进行临床试验，以比较不同的通气氧水平对心脏骤停后神经系统结局的影响。

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