Alkalinization during re-oxygenation prevents functional damage by hyperglycaemic hypoxia

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.