[Effect of xanthinol nicotinate on brain metabolism in rats].

The influence of 7-[2-hydroxy-3-(N-2-hydroxyethyl-N-methylamino)propyl]-1, 3-dimethyl-xanthine-pyridine-3-carboxylate (xantinol nicotinate, Complamin) on brain metabolism was studied in the following test models: 1. determination of glucose-14C permeation in rats with experimental nephrogenic hypertension; 2. determination of the intercerebral ATP-concentration in ischaemic rats; 3. determination of the adenosine triphosphate (ATP) pool in healthy rats; 4. evaluation of the incorporation rates of 32Pi-isotope into the adenosine phosphates of the rat brain. The results of these studies show, that the reduced glucose permeation rates in rats with nephrogenic hypertension can be normalized by xantinol nicotinate above values of controls. In hypoxemic rats it could be shown, that xantinol nicotinate antagonizes the decrease of the intracerebral ATP-concentration by 50%. The investigation of the ATP-pool resulted in a significant increase of the ATP level in the brain tissue about 35% at maximum. This increase of the ATP-concentration continues up to 4 h following a single oral administration of xantinol nicotinate. The determination of the incorporation rates of 32Pi-isotope showed that only small amounts of radioactivity were measured in the AMP-fraction in controls as well as in xantinol nicotinate treated rats. Further phosphorylation steps of adenosine monophosphate (AMP) to adenosine diphosphate (ADP) and ATP, however, are considerably activated by xantinol nicotinate, whereby maximum labelling rates of the ADP were found already 15 min after dosing. Maximum 32Pi-incorporation rates of the ATP-fraction were measured 30 min following administration of the tracer and of xantinol nicotinate, respectively.