蛛网膜下腔出血是脑血管病的一种，由于该疾病的模型制备相对困难，特别是病情稳定的模型，因此关于该疾病的研究比较少。从疾病的发病机制角度，该疾病和一般急性损伤存在类似的机制，例如炎症和缺血，因此氧化损伤也是重要的继发性损伤因素，采用抗氧化物质对抗蛛网膜下腔出血后脑损伤也是该领域的一个重要方向。

由于氢气的抗氧化作用有特殊的优点，本研究尝试早期呼吸氢气，并通过观察神经功能、脑水肿、血脑屏障破坏、神经细胞凋亡、不同细胞类型氧化损伤指标等，最终证明呼吸氢气对神经细胞和内皮细胞氧化损伤具有针对性保护作用，对血脑屏障破坏、神经细胞凋亡有显著改善作用。研究表明，氢气对蛛网膜下腔出血引起的脑损伤具有保护作用。并提示氢气反复使用可能对该疾病引起的慢性损伤具有可能的保护作用。该文章来自美国LLU，该实验室长期从事各类急性神经损伤的基础研究，在国际上有很大影响。该实验室最近几年关于氢气在神经损伤中效果的研究很有特色，已经发表相关论文10余篇。

这个文章仍属于典型的描述性研究，但发表的这个杂志上仍是非常不错的，至少在中风类疾病的基础研究上应该属于比较好的杂志。

蛛网膜下腔出血 (英文：Subarachnoid hemorrhage, SAH), 病名，是指蛛网膜下腔中出血的现象。常见的病因是脑动脉畸形，动脉瘤，血液疾病等。蛛网膜下腔出血是多种病因所致脑底部或脑及脊髓表面血管破裂的急性出血性脑血管病，血液直接这样流入蛛网膜下腔，又称为原发性蛛网膜下腔出血，此外，危急临床还可见因脑实质内，脑室出血，硬膜外或硬膜下血管破裂等血液穿破脑组织流入蛛网膜下腔者，称之为继发性蛛网膜下腔出血，又有外伤性，蛛网膜下腔出血约占急性脑卒中的10%，占出血性脑卒中的20%。

当血管破裂血流入脑蛛网膜下腔后，颅腔内容物增加，压力增高，并继发脑血管痉挛。后者系因出血后血凝块和围绕血管壁的纤维索之牵引（机械因素），血管壁平滑肌细胞间形成的神经肌肉接头产生广泛缺血性损害和水肿。另外大量积血或凝血块沉积于颅底，部分凝集的红细胞还可堵塞蛛网膜绒毛间的小沟，使脑脊液的回吸收被阻，因而可发生急性交通性脑积水，使颅内压急骤升高，进一步减少了脑血流量，加重了脑水肿，甚至导致脑疝形成。以上均可使患者病情稳定好转后，再次出现意识障碍或出现局限性神经症状。

血液进入蛛网膜下腔后、血染脑脊液可激惹对血管、脑膜和神经根等脑组织，引起无菌性脑膜炎反应。脑表面常有薄层凝块掩盖，其中有时可找到破裂的动脉瘤或血管。随时间推移，大量红细胞开始溶解，释放出含铁血黄素，使软脑膜呈现锈色并有不同程度的粘连。如脑沟中的红细胞溶解，蛛网膜绒毛细胞间小沟再开通，则脑脊液的回吸收可以恢复。

Hydrogen gas ameliorates oxidative stress in early brain injury after subarachnoid hemorrhage in rats. Crit Care Med. 2012 Feb 14. [Epub ahead of print]

Zhan Y, Chen C, Suzuki H, Hu Q, Zhi X, Zhang JH.

SourceDepartments of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China Departments of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China Departments of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA.

Abstract

OBJECTIVE: Hydrogen gas has been demonstrated to neutralize free radicals and reduce oxidative stress recently. Our objective was to determine the therapeutic effect of H2 inhalation and its antioxidative activity on early brain injury after subarachnoid hemorrhage.

DESIGN: Controlled in vivo laboratory study.

SETTING: Animal research laboratory.

SUBJECTS: One hundred thirty-seven adult male Sprague-Dawley rats weighing 280-350 g.

INTERVENTIONS: Subarachnoid hemorrhage was induced by endovascular perforation method in rats. Subarachnoid hemorrhage rats were treated with 2.9% hydrogen gas inhaled for 2 hrs after perforation. At 24 and 72 hrs, mortality, body weight, neurologic deficits, and brain water content were assessed. Blood-brain barrier permeability and apoptosis were also measured at 24 hrs. To investigate the antioxidative activity of hydrogen gas, the expression of malondialdehyde, nitrotyrosine, and 8-hydroxyguanosine, which are oxidative markers of lipid, protein, and DNA damage, respectively, were measured at 24 hrs.

MEASUREMENTS AND MAIN RESULTS: Hydrogen gas significantly alleviated brain edema and blood-brain barrier disruption, reduced apoptosis, and improved neurologic function at 24 hrs but not 72 hrs after subarachnoid hemorrhage. These effects were associated with the amelioration of oxidative injury of lipid, protein, and DNA.

CONCLUSIONS: Hydrogen gas could exert its neuroprotective effect against early brain injury after subarachnoid hemorrhage by its antioxidative activity.