Brain Lipid Changes Following Hypoxia

Abstract

Biochemical changes signaling irreversible damage in brain cells following hypoxia are incompletely understood. Disruption of membrane structure may play a role in this process. Lipids and long-chain fatty acids are important constituents of neural membranes and could serve as markers of membrane breakdown. The present study was undertaken to assess the brain lipid profile and the process of fatty acid elongation in adult rats subjected to hypoxia and unilateral carotid ligation. Following functional recovery from hypoxia, the brain lipids were analyzed in both hemispheres and disclosed a significant reduction of inositide glycerophosphatide (PI) and serine glycerophosphatide (PS). Mitochondrial fatty acid elongation was increased by more than 100% and the pattern of elongation more closely resembled that seen during myelination rather than maturity. Although the degree of brain hypoxia is not predictable in the rat model, the lipid alterations indicate a reparative process following a suppression of lipid metabolism during hypoxia. Delineation of biochemical processes signaling irreversible brain damage will await further studies on regional and subcellular changes.