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急性脑梗死约占全部脑卒中的70%，病死率和致残率高，且极易复发。但目前针对急性脑梗死在时间窗内溶栓、抗凝等治疗手段不能从根本上切实有效地修复受损脑组织，且伴有出血等风险。寻找脑梗死形成发展的原因并予以治疗迫在眉睫。酸中毒是引起缺血性脑损伤的重要机制。大量实验研究表明，酸中毒能加重神经元的缺血性损伤，且其梗死面积与酸中毒的程度直接相关。但缺血产生的酸中毒如何引起神经元损伤的确切机制尚不明确。最近研究发现酸中毒能激活一种在中枢及周围神经中广泛存在的膜通道，即酸敏感离子通道，它对Ca2+通透，能引起细胞内Ca2+超载，同时能激活胞内酶引起细胞内蛋白质、脂类及核酸的降解，加重缺血后脑损伤。本文就酸敏感离子通道1a 与脑梗死做一综述。

英文摘要:

Cerebral ischemia is a leading cause of death and long-termdisabilities which accounted for 70%of stroke, and it easy to relapse. Unfortunately, Current clinical practices for acute cerebral infarction utilize thrombolytic anticoagulation cannot fundamentally repair the damaged issue, and accompany with risk of bleeding. Looking for cerebral infarction etiology and treatment is urgent. Acidosis is a common feature in cerebral ischemia and was known to cause brain injury. The mechanisms were, however, unclear. The finding that Acid-sensing Ion Channels are highly enriched in brain neurons, their activation by ischemic acidosis, and their demonstrated Ca2+ permeability, excessive accumulation of Ca2+ in neurons leads to uncontrolled activation of various enzymes causing breakdown of proteins, lipids, and nucleic acids, aggravate the destruction of neurons. The article reviews the relation ASIC1a and Ischemic Brain Injury.

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