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Biomedical subjects

F Karoum

Publications and source records attributed to F Karoum.

At least 145 records · Page 8Linked to original sources
PubMed1977

The metabolism of biogenic amines in experimental animals and in human subjects during acute and chronic administration of ethanol.

Ethanol has been shown to induce a shift in catecholamine metabolism peripherally from normally oxidative pathways to reductive pathways. The mechanisms of this effect may result from competitive inhibition of aldehyde dehydrogenase by acetaldehyde. The shift in metabolism cannot be found in brain and alterations in catecholamine function may reflect changes in the turnover of these amines.

Acetaldehyde↗
PubMed1976

Brain concentrations of biogenic amine metabolites in acutely treated and ethanol-dependent rats.

1 Mass fragmentography was used to measure whole brain concentrations of some of the major metabolites of tyramine, octopamine, dopamine and noradrenaline in acutely treated and in ethanol-dependent rats. 2 Treatments with ethanol, either acutely or chronically, failed to alter significantly brain concentration of p-hydroxphenylacetic and p-hydroxymandelic acid (metabolites derived from tyramine and octopamine respectively). The effect on catecholamine metabolites was marked and therefore suggests that ethanol is selective in its effect on central metabolism of biogenic amines. 3 Acute ethanol treatment significantly increased brain concentration of homovanillic acid (HVA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylglycol (MHPG). Vanilmandelic acid (VMA) was not affected. All four metabolites (HVA, DOPAC, MHPG and VMA) were increased in the brains of rats rendered dependent on ethanol while still intoxicated (blood ethanol levels above 200 mg/dl). In ethanol-dependent rats undergoing ethanol withdrawal syndrome (no ethanol present in blood), the brain concentrations of HVA and DOPAC were normal while those of MHPG and VMA continued to be elevated. 4 From the decline in the concentrations of HVA and DOPAC after 50 mg pargyline/kg in control rats and rats acutely treated with ethanol, it was concluded that ethanol has no effect on the transport of phenolic acids across the blood brain barrier. 5 No reversal in the metabolism of catecholamines from an oxidative to a reductive pathway, analogous to that produced by ethanol in the periphery, could be established in the brain. 6 The increase in catecholamine metabolite concentrations after ethanol treatment, either acute or chronic, were interpreted as manifestations of increases catecholamine turnover.

Animals↗
PubMed1976

The effect of probenecid on the free and conjugaed 3-methoxy-4-hydroxyphenylglycol (MHPG) in lumbar cerebrospinal fluid.

Free and conjugated lumbar cerebrospinal fluid 3-methoxy-4-hydroxyphenylglycol (MHPG) was measured before and after probenecid treatment in 12 schizophrenic patients by a gas liquid chromatography-mass fragmentographic procedure. Neither the free nor conjugated MHPG was appreciably altered by probenecid. Total MHPG was statistically increased by probenecid but not to the point that the probenecid test would be clinically useful for estimating norepinephrine turnover from probenecid-induced changes in MHPG concentrations.

3-Methoxy-4-hydroxyphenylethanol↗
PubMed1975

Urinary phenolic acid and alcohol excretion in the newborn.

Mean urinary excretion values of some phenolic acids and alcohols have been measured by gas chromatography in 44 neonates (36 males, 6 females) during the first 2 days and days 3-7 of life, and the effect of prematurity and jaundice assessed. 4-Hydroxy-3-methoxymandelic acid (VMA) output rises immediately after birth in term but not in preterm infants. A similar increase in homovanillic acid (HVA) output was restricted to nonjaundiced term babies; in nonjaundiced preterm babies there was a steady rise during the first week. The ratio of HVA to VMA output was higher in these infants than in adults, suggesting a more rapid turnover of dopamine than adrenaline and noradrenaline. Unlike adult values, both HVA and VMA excretion values were directly related to urine volume, an observation perhaps related to renal immaturity. An unexplained reduction in HVA output in jaundiced as opposed to nonjaundiced infants was observed in the first 2 days of life. The ratio of 4-hydroxy-3-methoxyphenylglycol to VMA was about the same as in the adult. p-Hydroxyphenyl-lactic acid (p-HPLA), because of its superior stability, was measured in preference to p-hydroxyphenylpyruvic acid as an index of tyrosyluria. An output of 1 mg p-HPLA/24 h is proposed as the upper limit of normal. Prematurity was associated with a significant rise in p-HPLA output. A dramatic increase in excretion of this acid was noted in jaundiced, compared with nonjaundiced infants, presumably a manifestation of general enzyme immaturity.

Alcohols↗