Thiringer K, Blomstrand S, Hrbek A, Karlsson K, Kjellmer I
Brain Res. 1982 May 6;239(1):107-17. doi: 10.1016/0006-8993(82)90836-8.
Hypoxanthine (HX) and lactate are degradation products from energy-rich intracellular substrates (ATP and glycogen), and their concentration will increase during anaerobic conditions, such as fetal asphyxia. In this study the accumulation of the two metabolites in blood during asphyxia was studied in 7 acutely exteriorized fetal lambs. The arterio-venous difference of HX and lactate over the brain was related to the function of the fetal brain as reflected by the somato-sensory evoked electroencephalogram potentials (SEP). Increased concentrations of HX in plasma and lactate in blood occurred simultaneously with deterioration of the SEP and the 3 variables correlate highly significantly. During normoxia, a net cerebral influx was found for HX, which in combination with severe asphyxia gradually changed to a net efflux. A linear correlation was found between the cerebral arterio-venous differences of HX and the impairment of the SEP. No such correlation existed for lactate. The results suggest, that the fetal brain has a high threshold for degrading its energy-rich intracellular purines.