Effect of pyridoxine, glyoxylic acid and pyridoxylate on oxidative metabolism in vitro and phosphorylated energy-rich compounds studied in rat brains during acute hypoxia and ischaemia.

Pyridoxine (1-8 mmol/l) did not change significantly the cerebral oxygen nor the hypoxic or ischaemic degradation of phosphocreatine and ATP. Glyoxylic acid (1-8 mmol/l), an inhibitor of the citric acid cycle, depressed the electrically stimulated oxygen uptake of brain slices to a lesser extent than did pyridoxylate. Moreover, at concentrations of 0.66 mmol/l, pyridoxylate predominantly delayed the hypoxic or the ischaemic breakdown of creatine phosphate and of ATP compared with glyoxylic acid (0.66 mmol/l). These findings paralleled clearly the prominent hypoxic and post-hypoxic protection afforded by pyridoxylate upon rat brain electrogenesis, reported in the preceding paper.