Lascola C, Kraig R P
Department of Neurology, University of Chicago, IL 60637, USA.
Neurosci Biobehav Rev. 1997 Mar;21(2):143-50. doi: 10.1016/s0149-7634(96)00004-8.
Biochemical, histological, and physiological evidence suggest strongly that astrocytes may either defend or damage brain tissue, depending on the brain carbohydrate content preceding global ischemia (28,43). This paper will first review the concept of acidosis in ischemia and the possible role of severe, compartmentalized astrocytic acidosis in pan necrosis. Results are then presented demonstrating that astrocytes are also capable of maintaining an alkaline intracellular pH (pHi) during normoglycemic global ischemia. Mechanisms underlying depolarization-dependent astroglial alkalosis are then reviewed. Recent experiments indicate that bicarbonate (HCO3-) transport is a major mechanism by which astroglia not only alkalinize their interior but also acidify the interstitium. Maintenance of alkalosis during normoglycemic ischemia supports the hypothesis that astroglial HCO3- transport might ultimately protect neurons from excitotoxicity in ischemia without infarction (17). Inhibition of astroglial HCO3- transport may be a critical and requisite event, ultimately leading to compartmentalized astroglial acidosis and irreversible injury to all cell types.
生物化学、组织学和生理学证据有力地表明，星形胶质细胞可能保护或损害脑组织，这取决于全脑缺血前脑内碳水化合物的含量（28,43）。本文将首先回顾缺血中酸中毒的概念以及严重的、局部性星形胶质细胞酸中毒在全脑坏死中可能发挥的作用。随后展示的结果表明，在正常血糖性全脑缺血期间，星形胶质细胞也能够维持细胞内碱性pH值（pHi）。接着回顾了去极化依赖性星形胶质细胞碱化的潜在机制。最近的实验表明，碳酸氢根（HCO3-）转运是星形胶质细胞不仅使细胞内碱化而且使细胞间质酸化的主要机制。在正常血糖性缺血期间维持碱化支持了这样一种假说，即星形胶质细胞的HCO3-转运最终可能保护神经元免受缺血而非梗死时的兴奋毒性作用（17）。抑制星形胶质细胞的HCO3-转运可能是一个关键且必要的事件，最终导致局部性星形胶质细胞酸中毒以及对所有细胞类型的不可逆损伤。
