Astroglial acid-base dynamics in hyperglycemic and normoglycemic global ischemia.

Journal Article (Journal Article;Review)

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.

Full Text

Duke Authors

Cited Authors

  • Lascola, C; Kraig, RP

Published Date

  • March 1997

Published In

Volume / Issue

  • 21 / 2

Start / End Page

  • 143 - 150

PubMed ID

  • 9062937

Pubmed Central ID

  • PMC2810266

International Standard Serial Number (ISSN)

  • 0149-7634

Digital Object Identifier (DOI)

  • 10.1016/s0149-7634(96)00004-8

Language

  • eng

Conference Location

  • United States