The determination of inosine and hypoxanthine in the rat brain during normothermic and hypothermic anoxia.

Abstract

Since hypoxanthine and xanthine are metabolized by xanthine oxidase to urate in the presence of an adequate oxygen supply, the concentration of the precursors of urate may be used as markers of the oxygen supply to the central nervous system. the present paper intends to elucidate this question. Brain anoxia was induced in rats by decapitation. the purine metabolites inosine (hypoxanthine-riboside) and hypoxanthine were determined in brain-tissue following anoxia which lasted from 1 min up to 24 h. A new method for the determination of hypoxanthine in plasma was modified for the determination of these metabolites in brain tissue. This method has been evaluated with regard to precision and recovery. The hypoxanthine level was significantly augmented after 8 min of normothermic (37°C) anoxia compared to control values. A steady increase in the concentration of this metabolite was found up to 24 h of anoxia, although the rate of increase tapered off after approximately 30 min of anoxia. A similar pattern was found with regard to alteration in inosine concentrations. the inosine level was, however, significantly increased compared to the control level already after one minute of anoxia. During hypothermic (29°C) anoxia up to 2 h, the increase of brain tissue hypoxanthine concentration was slower compared to values found during normothermic anoxia. It is concluded that measurements of these metabolites in brain tissue are useful indicators of the degree of brain tissue hypoxia.