Abstract
Ischaemic brain injury was induced in rats and the oxygen consumption of brain homogenates was measured 1-4 hr afterwards.
In animals with severe enough brain damage to produce fits in vivo, in vitro respiration was reduced below control values.
Potentiation of oxygen uptake by ischaemic homogenates in vitro was produced by succinate, lactate, malate and adenosine diphosphate. Inhibition was produced by adenosine triphosphate. It is suggested that a deficiency of tricarboxylic acid intermediates contributes to the biochemical lesion in the ischaemic tissue, but there is no evidence of respiratory uncoupling.
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Selected References
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