Aspects of influx and efflux of homovanillic acid of rat cerebrospinal fluid.

In rats, different methods of perfusion (lumbar-cisternal or ventricular-cisternal) with artificial cerebrospinal fluid were performed at velocities of about 30 and 180 microliter/min. Levels of homovanillic acid (HVA) in the outflow were assayed with a semiautomated fluorimetric technique. Intravenous administration of 20 microgram HVA did not substantially enhance the outflow of this acid, indicating that in our preparations HVA found in the perfusate is of central origin. In the lumbar-cisternal preparation probenecid (200 mg/kg, i.p.) was found to inhibit the efflux of a significant fraction of HVA added to the medium, at both perfusion rates. The proportions of HVA eliminated by a probenecid sensitive transport was much higher at the lower rate of perfusion. Following probenecid the increase of endogenous HVA in the ventricular-cisternal perfusate was higher at a lower rate of perfusion. We determined the turnover rate of HVA in the whole brain and compared this value with the HVA outflow in the various preparations. The highest efflux of HVA was found in the ventricular-cisternal preparation during probenecid treatment and did not appear to be dependent upon the rate of perfusion. A maximal value of 3.5% of HVA formed in the central nervous system was found to be released into the cerebrospinal fluid.