The influence of acute ethanol on the catecholamine system in man as reflected in cerebrospinal fluid and urine. A new condensation product, 1-carboxysalsolinol.

Urine and cerebrospinal fluid (CSF) were collected from 10 healthy male volunteers after ingestion of 120 g ethanol and under similar conditions without ethanol. Dopamine (DA), homovanillic acid (HVA), norepinephrine (NE), 4-hydroxy-3-methoxyphenylglycol (HMPG), 4-hydroxy-3-methoxymandelic acid (HMMA = VMA), 1-carboxysalsolinol (1-CSAL), salsolinol (SAL) and methylated salsolinol (M-SAL) were analyzed with gas chromatography-mass spectrometry. In CSF collected 6 h after ethanol intake the concentration of NE and its metabolite HMPG were significantly elevated (P less than 0.025 and P less than 0.005, respectively) compared to control conditions. The other compounds analyzed did not change significantly. In urine collected during 10 h after ethanol administration the excretion of HMMA was significantly reduced (P less than 0.01) and the HMPG/HMMA ratio was significantly elevated (P less than 0.005) reflecting a change in the peripheral red-ox state during ethanol oxidation. The excretion of DA and its major metabolite HVA did not change. However, the DA-derived condensation products 1-CSAL (from DA and pyruvate) increased (P less than 0.001), while SAL (from DA and acetaldehyde) decreased (P less than 0.005) after ethanol ingestion compared to the control situation. The increased excretion of 1-CSAL indicated that the ethanol metabolism interferes with the glucose metabolism, probably through an acetaldehyde-mediated inhibition of the pyruvate dehydrogenase complex.