蛛网膜下腔出血后早期脑损伤及神经保护治疗的研究进展

Advances in research on early brain injury and therapeutic options for neuroprotection following subarachnoid hemorrhage

蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后早期脑损伤(early brain injury,EBI)与迟发性脑损伤及患者的预后密切相关。关于EBI分子机制的研究表明,SAH后脑组织内微血管改变、离子失衡、血脑屏障损伤、免疫炎症反应、氧化应激、细胞死亡通路激活等多种病理机制共同导致神经血管功能障碍。这些研究进展为SAH后神经功能保护提供了多个可能的干预靶点,其中钙通道拮抗剂、内皮素-1受体阻滞剂、抗血小板药物、抗炎药物以及抗氧化应激药物等可能对SAH后EBI具有神经保护作用。进一步阐明SAH后脑缺血缺氧性损伤、神经免疫炎症激活、皮层传播抑制、各种细胞信号通路激活等脑损伤的相关分子机制以及这些诸多复杂的病理生理过程发生演变的规律,将对减轻SAH后脑损伤,促进神经修复,提高患者生存率与生存质量具有重要意义。

Early brain injury （EBI） and delayed cerebral injury following subarachnoid hemorrhage （SAH） are closely associated with poor prognosis in patients. Studies on the molecular mechanisms of EBI have revealed several pathological mechanisms involved in neurovascular dysfunction. These mechanisms include microvascular changes, altered ionic homeostasis, blood-brain barrier disruption, inflammation, oxidative stress, and cell death pathway activation. These studies also provide multiple possible intervention targets for protecting neurological function after SAH, in which calcium channel blockers, endothelin-1 antagonism, anti-platelet agents, anti-inflammatory agents, and antioxidants may have neuroprotective effects against EBI. Further elaborating on the molecular mechanisms of SAH-induced hypoxic-ischemic brain injury, neuroinflammation, cortical spreading depression, neuronal cell death and revealing the evolvement of these complex pathophysiological processes are of great significance for reducing brain injury after SAH, promoting nerve repair, and ameliorating patients＇ quality of life and overall mortality.