Dogs were subjected to cerebrospinal fluid (CSF) convexity-cisternal perfusion with [U-14C]adenosine, [U-14C]inosine, or [U-14C]hypoxanthine to determine the mechanism of incorporation of these purines into brain adenine nucleotides. After craniotomy, brain tissue was frozen in situ, and the adenine nucleotides were separated by chromatography. A portion of the nucleotide fraction from the brain and [U-14C]purine from CSF were hydrolyzed enzymatically to nucleosides and bases and the specific activities (SA) measured. The pathway of incorporation of adenosine and inosine was determined by comparing the ratio of SA nucleoside to SA base obtained from degraded brain to that obtained from degraded CSF. Adenosine was directly phosphorylated to AMP, but inosine was degraded before incorporation into brain nucleotides. By comparing the SA of the brain nucleotides to that of the purine precursor in the cerebral spinal perfusion fluid, the incorporation of adenosine was found to be sevenfold greater than that of inosine or hypoxanthine. Measurement of the radioactivity in sagittal venous blood during the convexity-cisternal perfusion yielded a larger percentage of counts after perfusion with [U-14C]inosine than with adenosine or hypoxanthine. In comparison to other tissues, a unique salvage system thus exists in the brain for adenosine that serves to conserve the adenine nucleotide pool.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1980|