Department of Neurosurgery, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang, China.
J Neurosci Res. 2012 Aug;90(8):1670-80. doi: 10.1002/jnr.22739. Epub 2012 May 15.
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 (H(2)) can selectively reduce levels of hydroxyl radicals (·OH) and ameliorate oxidative and inflammatory injuries to organs in many models. However, whether H(2) can ameliorate CV after SAH is still unknown. This study was designed to evaluate the efficacy of H(2) 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 H(2) 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.
脑血管痉挛（CV）仍然是蛛网膜下腔出血（SAH）患者常见且严重的并发症。尽管其具有临床意义且已进行广泛研究，但 CV 的潜在发病机制和治疗观点仍不完全清楚。最近，有研究表明，分子氢（H₂）可以选择性地降低羟基自由基（·OH）的水平，并改善许多模型中的器官氧化和炎症损伤。然而，H₂是否可以改善 SAH 后的 CV 尚不清楚。本研究旨在评估 H₂预防 SAH 后 CV 的疗效。通过枕骨大池内注射血液来诱导 Sprague-Dawley 大鼠实验性 SAH。在损伤后立即和 24 小时经腹腔内注射富氢盐水（HS）（5 ml/kg）。在 SAH 后记录神经功能检查评分后 48 小时处死所有大鼠。评估氧化应激和炎症水平。通过光镜和透射电镜检查基底动脉的组织学检查来评估血管痉挛情况。HS 治疗可显著改善神经功能预后，并减轻 SAH 后基底动脉的形态学血管痉挛。此外，我们发现 HS 治疗对 SAH 后 CV 的有益作用与基底动脉中脂质过氧化水平降低、抗氧化酶活性增加和促炎细胞因子水平降低有关。这些结果表明，H₂具有成为治疗 SAH 后 CV 的新型治疗策略的潜力，其神经保护作用可能部分通过限制血管炎症和氧化应激来介导。
