Oxygen dependency of cerebral oxidative phosphorylation in newborn piglets

Changes in hemoglobin oxygenation and oxidation state of the Cu-A centre of cytochrome oxidase were measured with full spectral near infrared spectros copy simultaneously with phosphorus metabolites using nuclear magnetic reso nance P-31 spectroscopy at high time resolution (10 seconds) during transie nt anoxia (F(i)o(2) = 0.0 for 105 seconds) in the newborn piglet brain. Dur ing the onset of anoxia, there was no change in either phosphocreatine (PCr ) concentration or the oxidation state of the Cu-A centre of cytochrome oxi dase until there was a substantial fall in cerebral hemoglobin oxygenation. at which point the Cu-A centre reduced simultaneously with the decline in PCr. At a later time during the anoxia, intracellular pH decreased rapidly, consistent with a fall in cerebral metabolic rate for O-2 and reduced nux through the tricarboxylic acid cycle. The simultaneous reduction of Cu-A an d decline in PCr san be explained in terms of the effects of the falling mi tochondrial electrochemical potential. From these observations, it is concl uded that, at normoxia, oxidative phosphorylation and the oxidation state o f the components of the electron transport chain are independent of cerebra l oxygenation and that the reduction in the Cu-A signal occurs when oxygen tension limits the capacity of oxidative phosphorylation to maintain the ph osphorylation potential.