Euchner-Wamser, Ingrid; Grafe, Peter; Sennefelder, Elke; Schneider, Uwe
Alkalinization during re-oxygenation prevents functional damage by hyperglycaemic hypoxia. Membrane and Cellular Biophysics and Biochemistry.
In: Neuroreport, Vol. 5, No. 13: pp. 1574-1576
HYPERGLYCAEMIA impairs recovery from transient cerebral ischaemia: the importance of tissue acidification for this phenomenon has not been clarified in detail. We investigated this issue in a less complex in vitro preparation of isolated rat dorsal spinal roots exposed for 30 min to hyperglycaemic hypoxia. Peak height of compound action potentials recovered minimally in 5 mM bicarbonate. However, recovery was greatly improved by addition of the weak base trimethylamine during re-oxygenation. Addition of the weak acid propionate had no such effect. Cytoplasmic alkalinization improved recovery in a brief time window only: application of trimethylamine after 15 min of re-oxygenation was without beneficial effect. These data emphasize the importance of cytoplasmic acidification for neurophysiological recovery from hyper-glycaemic hypoxia during the initial period of re-oxygenation.