中风有三种类型，脑血管血栓或拴塞引起的脑梗死是脑组织缺血性病变；脑组织内血管出血的脑出血性改变；脑表面血管破裂引起的蛛网膜下腔出血。在这些类型中，缺血的发病率最高，但死亡率比较低，脑出血和蛛网膜下腔出血发病率比较低，但死亡率非常高。过去学术界对脑缺血的研究比较多，现在对脑出血和蛛网膜下腔出血的研究也逐渐增多。

蛛网膜下腔出血 (英文：Subarachnoid hemorrhage, SAH)，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，血液直接流入蛛网膜下腔，又称为原发性蛛网膜下腔出血。常见的病因是脑动脉畸形、动脉瘤、血液疾病等。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。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%。凡能引起脑出血的病因也能引起本病，但以颅内动脉瘤、动静脉畸形、高血压动脉硬化症、脑底异常血管网（moya-moya病）和血液病等为最常见。多在情绪激动或过度用力时发病。动脉瘤好发于脑底动脉环的大动脉分支处，以该环的前半部较多见。动静脉畸形多位于大脑半球大脑中动脉分布区。

在氢气和中风关系的研究中，对脑缺血的研究已经非常多，对脑出血的研究相对比较少，不过对蛛网膜下腔出血的研究目前已经有3篇文章报道。其中一篇来自美国，是呼吸氢气对早期脑损伤的效果研究，另一篇来自南京大学，是关于神经细胞凋亡的研究。这里又有一来自浙江大学附属医院神经外科的文章，是关于蛛网膜下腔出血后血管痉挛的效果观察。

脑出血特别是蛛网膜下腔出血后，血管痉挛也是临床上非常棘手的问题。其原因并不十分清楚，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。一般认为，血管痉挛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。由于血管痉挛可以导致继发性脑组织缺血，加重病情，因此研究蛛网膜下腔出血不得不关注这个重要问题。本研究证明，氢气生理盐水注射可以减少血管痉挛的发生。

Beneficial effect of hydrogen-rich saline on cerebral vasospasm after experimental subarachnoid hemorrhage in rats

Yuan Hong1,†,

Songxue Guo1,†,

Sheng Chen

Abstract

Cerebral vasospasm (CV) remains a common and devastating complication in patients with subarachnoid hemorrhage (SAH). Despite its clinical significance and extensive research, the underlying pathogenesis and therapeutic perspectives of CV remain incompletely understood. Recently, it has been suggested that molecular hydrogen (H2) can selectively reduce levels of hydroxyl radicals (·OH) and ameliorate oxidative and inflammatory injuries to organs in many models. However, whether H2 can ameliorate CV after SAH is still unknown. This study was designed to evaluate the efficacy of H2 in preventing SAH-induced CV. Experimental SAH was induced in Sprague-Dawley rats using cisterna magna blood injection. Hydrogen-rich saline (HS) was injected intraperitoneally (5 ml/kg) immediately and at 24 hr after injury. All rats were sacrificed 48 hr after the neurological examination scores had been recorded following SAH. Levels of oxidative stress and inflammation were evaluated. Basilar artery vasospasm was assessed by histological examination using light and transmission electron microscopy. HS treatment significantly improved neurological outcomes and attenuated morphological vasospasm of the basilar artery after SAH. In addition, we found that the beneficial effects of HS treatment on SAH-induced CV were associated with decreased levels of lipid peroxidation, increased activity of antioxidant enzymes, and reduced levels of proinflammatory cytokines in the basilar artery. These results indicate that H2 has the potential to be a novel therapeutic strategy for the treatment of CV after SAH, and its neuroprotective effect might be partially mediated via limitation of vascular inflammation and oxidative stress. © 2012 Wiley Periodicals, Inc.