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Brooks, K.J. et al.

Brooks, Hargreaves, Bhakoo, Sellwood, O'Brien, Noone, Sakata, Cady, Wylezinska, Thornton, Ordidge, Nguyen, Clemence, Wyatt, Bates,

Delayed hypothermia prevents decreases in N-acetylaspartate and reduced glutathione in the cerebral cortex of the neonatal pig following transient hypoxia-ischaemia.

The effects of normothermia and delayed hypothermia on the levels of N-acetylaspartate (NAA), reduced glutathione (GSH) and the activities of mitochondrial complex I, II-III, IV and citrate synthase were measured in brain homogenates obtained from anaesthetized neonatal pigs following transient in vivo hypoxia-ischaemia. In the normothermic animals there was a significant decrease in complex I activity and in the levels of GSH and NAA when compared to the controls. Delayed hypothermia preserved NAA and GSH at control levels and enhanced the rate of complex II-III activity. There was correlation (R = 0.79) between GSH and NAA levels when data from all three experimental groups were analyzed. Citrate synthase activity was not significantly different in the three groups, indicating maintenance of mitochondrial integrity. These data suggest that delayed hypothermia affords protection of integrated mitochondrial function in the neonatal brain following transient hypoxia-ischaemia.[1]

References

Delayed hypothermia prevents decreases in N-acetylaspartate and reduced glutathione in the cerebral cortex of the neonatal pig following transient hypoxia-ischaemia. Brooks, K.J., Hargreaves, I., Bhakoo, K., Sellwood, M., O'Brien, F., Noone, M., Sakata, Y., Cady, E., Wylezinska, M., Thornton, J., Ordidge, R., Nguyen, Q., Clemence, M., Wyatt, J., Bates, T.E. Neurochem. Res. (2002) [Pubmed]

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