呼吸氢气可以提高心脏骤停复苏后生存率

尽管在非创伤性心脏骤停处理方面有许多发展，但是心脏骤停的存活率依然很低，许多侥幸存活的患者经常会遗留神经系统和心脏功能异常的后遗症。心脏骤停复苏后综合症包括神经系统功能异常、心脏损伤和脓毒症样系统炎症等可导致多器官功能异常，并最终导致许多幸存者继发性死亡。低温治疗是被广泛接受的保护心脏骤停后损伤的金标准，研究表明低温治疗可以降低心脏骤停复苏后神经系统功能异常，提高患者存活率。但受到各种因素的限制，低温治疗方法并没有在临床上被全面使用，因此寻找替代和联合低温治疗方法仍是值得研究的课题。

分子氢作为一种新的抗氧化物质，自从2007年以来，大量关于氢气治疗疾病，如对心脏和脑缺血再灌注损伤等的动物实验被报道，也有许多初步的临床研究证明氢气在人体的生物学效应。

心脏骤停复苏后综合症是一种典型的全身器官缺血再灌注损伤。那么利用氢气对心脏骤停复苏后综合症非常有可能具有治疗作用。本研究正是基于这一假说开展的。

研究设计了4种动物分组，第1组是正常温度心脏骤停复苏；第2组是正常温度心脏骤停复苏呼吸2%氢气；第3组低温治疗；第4组低温联合呼吸2%氢气。所有治疗时间均为2小时。检测指标分别为动物生存率、神经系统功能评分、血清炎症因子IL-6水平检测、心脏氧化指标8-OHdG和4-HNE阳性细胞检测。研究结果表明，呼吸氢气的效果比低温治疗效果更好。非常有意思的是，呼吸氢气对早期（24小时内）存活率明显超过低温治疗，而且从对血清炎症因子的影响看，低温几乎没有效果，但氢气的效果非常明显。这一研究提示，将呼吸氢气作为一种挽救心脏骤停复苏患者生命的方法非常值得尝试。

氧气对维持生命的作用毋庸置疑，现在看来，氢气不仅可以治疗疾病，而且在关键时刻可以挽救患者生命。

    H2 Gas Improves Functional Outcome After Cardiac Arrest to an Extent Comparable to Therapeutic Hypothermia in a Rat Model

Kei Hayashida, MD;

Department of Emergency and Critical Care Medicine, Keio University, Tokyo, Japan (K.H., M. Suzuki, S.H.)

Correspondence to:

 Motoaki Sano, MD, PhD, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan. E-mail: msano@a8.keio.jp

Background All clinical and biological manifestations related to postcardiac arrest (CA) syndrome are attributed to ischemia–reperfusion injury in various organs including brain and heart. Molecular hydrogen (H2) has potential as a novel antioxidant. This study tested the hypothesis that inhalation of H2 gas starting at the beginning of cardiopulmonary resuscitation (CPR) could improve the outcome of CA.

Methods and Results Ventricular fibrillation was induced by transcutaneous electrical epicardial stimulation in rats. After 5 minutes of the subsequent CA, rats were randomly assigned to 1 of 4 experimental groups at the beginning of CPR: mechanical ventilation (MV) with 2% N2 and 98% O2 under normothermia (37°C), the control group; MV with 2% H2 and 98% O2 under normothermia; MV with 2% N2 and 98% O2 under therapeutic hypothermia (TH), 33°C; and MV with 2% H2 and 98% O2 under TH. Mixed gas inhalation and TH continued until 2 hours after the return of spontaneous circulation (ROSC). H2 gas inhalation yielded better improvement in survival and neurological deficit score (NDS) after ROSC to an extent comparable to TH. H2 gas inhalation, but not TH, prevented a rise in left ventricular end-diastolic pressure and increase in serum IL-6 level after ROSC. The salutary impact of H2 gas was at least partially attributed to the radical-scavenging effects of H2 gas, because both 8-OHdG- and 4-HNE-positive cardiomyocytes were markedly suppressed by H2 gas inhalation after ROSC.

Conclusions Inhalation of H2 gas is a favorable strategy to mitigate mortality and functional outcome of post-CA syndrome in a rat model, either alone or in combination with TH.