Abnormalities of cerebral blood flow during and following
hypoxia and
ischemia contribute to the progression of tissue injury. Oxidative stress during and following
hypoxia is known to markedly increase
superoxide anion concentration. There is conflicting evidence that the concentration of
superoxide anion regulates cerebral blood flow through its effect on vascular tone, although difficulties in measurement of
superoxide anion complicate these studies. In order to test the hypothesis that changes in cerebral blood flow during and following
hypoxia are due to changes in extracellular
superoxide anion levels, we examined tissue
oxygen levels by fiberoptic oximetry and
superoxide anion levels using a previously validated
cytochrome c coated
electrode on the cortical surface and correlated these measurements to cerebral blood flow measured by
laser Doppler in rats subjected to 20 min of
hypoxia followed by hyperoxic reoxygenation recovery. The results showed a burst of
superoxide anion with the onset of reoxygenation that temporally correlated with a transient peak in tissue
oxygen tension lasting 10 min. and was eliminated by pretreatment with
Cu-Zn superoxide dismutase conjugated to
polyethylene glycol. Cerebral blood flow did not differ during
hypoxia or recovery in the
polyethylene glycol conjugated
superoxide dismutase and control treatment groups. This study demonstrated no effect of increased
superoxide anion concentration on cerebral blood flow during hyperoxic recovery following
hypoxia.