TRANSPORT OF HYPOXANTHINE FROM PLASMA TO CEREBROSPINAL-FLUID AND VITREOUS-HUMOR IN NEWBORN PIGS

To determine whether an elevated level of hypoxanthine in cerebrospina l fluid or vitreous humor might reflect a high plasma hypoxanthine con centration, or whether it necessarily represents local tissue hypoxia, we infused hypoxanthine intravenously to normoxemic and normotensive piglets (n = 6). Hypoxanthine was measured in different body fluids us ing HPLC. During the 8 hours of infusion hypoxanthine increased in pla sma (from 30 +/- 6 mumol/l (mean +/- SD) before the infusion to 68 +/- 20 mumol/l at the end of the infusion, p < 0.01), cerebrospinal fluid (CSF) (19 +/- 8 to 43 +/- 9 mumol/l, p < 0.05) and vitreous humor (15 +/- 5 to 30 +/- 6 mumol/l, p < 0.05). After infusion, hypoxanthine va lues in all three fluids were similar to those seen in pigs after seve re hypoxia. Hypoxanthine in vitreous humor and plasma were significant ly correlated (r = 0.80, 95% confidence interval 0.47-0.93, p < 0.001) . Urinary excretion of hypoxanthine increased almost 40 times from 0.1 2 +/- 0.14 to 4.6 +/- 2.9 mumol/kg/h indicating that renal excretion o f hypoxanthine is not achieved just by passive filtration. We conclude that in newborn piglets hypoxanthine can pass from plasma to CSF and vitreous humor. Thus an increased CSF hypoxanthine concentration is no t definite proof that significant cerebral hypoxia has occurred.