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吸入高浓度氢气可减轻窒息诱导心脏骤停大鼠模型中的认知缺陷。

Inhalation of high-concentration hydrogen gas attenuates cognitive deficits in a rat model of asphyxia induced-cardiac arrest.

作者信息

Huang Lei, Applegate Ii Richard L, Applegate Patricia M, Gong Lei, Ocak Umut, Boling Warren, Zhang John H

机构信息

Department of Neurosurgery, School of Medicine, Loma Linda University, Loma Linda, CA, USA.

Department of Anesthesiology and Pain Medicine, School of Medicine, University of California, Davis, Sacramento, CA, USA.

出版信息

Med Gas Res. 2019 Jul-Sep;9(3):122-126. doi: 10.4103/2045-9912.266986.

DOI:10.4103/2045-9912.266986
PMID:31552874
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6779004/
Abstract

Cognitive deficits are a devastating neurological outcome seen in survivors of cardiac arrest. We previously reported water electrolysis derived 67% hydrogen gas inhalation has some beneficial effects on short-term outcomes in a rat model of global brain hypoxia-ischemia induced by asphyxia cardiac arrest. In the present study, we further investigated its protective effects in long-term spatial learning memory function using the same animal model. Water electrolysis derived 67% hydrogen gas was either administered 1 hour prior to cardiac arrest for 1 hour and at 1-hour post-resuscitation for 1 hour (pre- & post-treatment) or at 1-hour post-resuscitation for 2 hours (post-treatment). T-maze and Morris water maze were used for hippocampal memory function evaluation at 7 and 14 days post-resuscitation, respectively. Neuronal degeneration within hippocampal Cornu Ammonis 1 (CA1) regions was examined by Fluoro-Jade staining ex vivo. Hippocampal deficits were detected at 7 and 18 days post-resuscitation, with increased neuronal degeneration within hippocampal CA1 regions. Both hydrogen gas treatment regimens significantly improved spatial learning function and attenuated neuronal degeneration within hippocampal CA1 regions at 18 days post-resuscitation. Our findings suggest that water electrolysis derived 67% hydrogen gas may be an effective therapeutic approach for improving cognitive outcomes associated with global brain hypoxia-ischemia following cardiac arrest. The study was approved by the Animal Health and Safety Committees of Loma Linda University, USA (approval number: IACUC #8170006) on March 2, 2017.

摘要

认知缺陷是心脏骤停幸存者中出现的一种毁灭性神经学后果。我们之前报道过,水电解产生的67%氢气吸入对窒息性心脏骤停诱导的全脑缺氧缺血大鼠模型的短期结局有一些有益影响。在本研究中,我们使用相同的动物模型进一步研究了其对长期空间学习记忆功能的保护作用。水电解产生的67%氢气在心脏骤停前1小时给予1小时,并在复苏后1小时给予1小时(预处理和后处理),或者在复苏后1小时给予2小时(后处理)。分别在复苏后7天和14天使用T迷宫和莫里斯水迷宫评估海马记忆功能。通过离体荧光金染色检查海马角回1(CA1)区域内的神经元变性。在复苏后7天和18天检测到海马缺陷,海马CA1区域内的神经元变性增加。两种氢气治疗方案在复苏后18天均显著改善了空间学习功能,并减轻了海马CA1区域内的神经元变性。我们的研究结果表明,水电解产生的67%氢气可能是一种有效的治疗方法,可改善心脏骤停后全脑缺氧缺血相关的认知结局。该研究于2017年3月2日获得美国洛马林达大学动物健康与安全委员会批准(批准号:IACUC #8170006)。

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