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Concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were investigated by lumbar cerebrospinal fluid (CSF) of 21 patients with partial and total spinal subarachnoid block. HVA levels in CSF below a complete block were significantly lower and 5-HIAA levels were signigicantly higher than controls. Below a partial block, HVA levels were normal; 5-HIAA levels were higher than in patients with complete block. Possible explanations for these findings are discussed.
The accumulation of 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) in rat brain has been examined after probenecid infusion over 8 h. At plasma probenecid concentrations of 200-400 micrograms mL-1 a steady state level in the accumulation of 5-HIAA and HVA was achieved, the increase above the endogenous levels being 135% and 65%, respectively. When the plasma concentration of probenecid rose above 400 micrograms mL-1 there was further accumulation of both 5-HIAA and HVA probably induced by increased neuronal activity or toxicity due to probenecid. The explanation for the plateau of 5-HIAA and HVA obtained over the plasma probenecid concentration interval of 200-400 micrograms mL-1 could be that the levels were reached when there was complete inhibition of active transport, and when the rate of formation of the metabolites equalled the rate of elimination by alternative routes i.e. bulk flow and diffusion. Therefore when probenecid is used to inhibit the active transport of acid monoamine metabolites across the blood-brain barrier, its plasma concentration should be within the range of 200-400 micrograms mL-1.
The effects of application of five different stressors on extracellular 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in the striatum and hippocampus were compared using in vivo microdialysis. Forced swimming for 30 min elevated extracellular 5-hydroxytryptamine to 90% above basal levels and reduced 5-hydroxyindoleacetic acid to 45% of basal levels in the striatum during the swim session. In contrast, hippocampal 5-hydroxytryptamine was not altered significantly by forced swimming but 5-hydroxyindoleacetic acid levels were reduced to 60% of basal levels. Tail pinch for 5 min elevated 5-hydroxytryptamine to 55% above basal levels in striatum and to 35% above basal levels in hippocampus. Tail pinch had no effect on 5-hydroxyindoleacetic acid in either brain region. In contrast to forced swimming and the tail pinch, the other three stressors, immobilization stress for 100 min, exposure to a cold environment (4 degrees C) for 2 h, and forced motor activity on a rotarod for 30 min, failed to alter extracellular 5-hydroxytryptamine in either the striatum or the hippocampus. All five stressors increased plasma corticosterone levels: tail pinch, 246%; cold stress, 432%; immobilization, 870%; forced motor activity, 1030%; and forced swimming, 1530%. These results suggest that individual stressors produce different effects on extracellular 5-hydroxytryptamine in different brain regions. In addition, there does not appear to be a relationship between the effects of stressors on the 5-hydroxytryptamine system and the magnitude of their ability to activate the hypothalamic-pituitary-adrenal axis.
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The metabolite 5-hydroxyindoleacetic acid, the major metabolic product of serotonin, can be measured by reacting it with orthophthalaldehyde to form a highly fluorescent product. The inclusion of cysteine in this reaction causes an increase in the amount of fluorescence. The rate of fluorescence formation for reaction containing cysteine is much faster than the rate for the reaction without cysteine. The differences observed for both excitation and remission maxima between reaction products formed in the presence and absence of cysteine indicate that these products are different. Furthermore, the significant difference in the regression coefficients of fluorescence of the reaction products versus HC1 concentration adds further evidence that the reaction products formed in the presence and absence of cysteine are different. HC1 appears to influence the reaction of 5-HIAA, OPT and cysteine in several ways: by causing the destruction of 5-HIAA, by affecting the fluorescence of the product formed, and by influencing the amount of reaction product formed.
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Oral administration of L-tryptophan to rats produced two main biochemical and pharmacological effects: a marked increase in urinary 5-hydroxyindoleacetic acid excretion, and a significant reduction in the urine flow after a water load. Urinary 5-hydroxyindoleacetic acid excretion reached its maximum 2 to 6 hr after the administration of tryptophan, and it increased with the dose of the amino acid. Antidiuresis was seen after the administration of L-tryptophan, 200 mg/kg, or more. The effect appeared promptly and it was roughly proportional to the dose of the amino acid administered. Both antidiuretic effect and increase in urinary 5-hydroxyindoleacetic acid excretion were more intense after oral than after parenteral administration of L-tryptophan. D-Tryptophan, in oral doses up to 1,000 mg/kg, produced neither an increase in urinary 5-hydroxyindoleacetic acid nor a reduction of diuresis. Available evidence suggests that reduction of urine flow is a consequence of biosynthesis and release of 5-hydroxytryptamine by the gastrointestinal mucosa. Tryptamine produced by direct decarboxylation of L-tryptophan does not seem to play any important role.
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In cats, 19 days after the lower thoracic cord was injllred, the concentrations of 5-hydroxytryptamine and its metabolite 5-hydroxyindoleacetic acid in the lumbosacral cord and that of 5-hydroxyindoleacetic acid in the lumbar fluid decreased. At the same time the concentrations of these substances in the cord above the lesion and that of 5-hydroxyindoleacetic acid in the cisternal fluid was not significantly altered. Since high concentrations of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid are present in the human lumbosacral cord, it appears that the concentration of 5-hydroxyincdoleacetic acid in the lumbar fluid of animals and man reflects the biochemical changes of 5-hydroxytryptamine in the spinal cord.
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To study the purported role of central monoamine disturbances in the pathophysiology of the opsoclonus-myoclonus syndrome, the serotonin metabolite 5-hydroxyindoleacetic acid and the dopamine metabolite homovanillic acid were measured in cerebrospinal fluid samples from 27 affected children and 47 age- and gender-matched control subjects by high-pressure liquid chromatography with electrochemical detection. 5-Hydroxyindoleacetic acid and homovanillic acid concentrations in the cerebrospinal fluid were approximately 30 to 40% lower in opsoclonus-myoclonus patients compared to control subjects, and the normal inverse correlation between age and monoamine metabolite concentrations in the cerebrospinal fluid of control subjects was not found in opsoclonus-myoclonus patients. Patients with the lowest values were less than 4 years old, and a subgroup had extremely low levels, but differences in older children were not significant. Cerebrospinal fluid levels of 5-hydroxyindoleacetic acid and homovanillic acid were more positively correlated in control subjects than in opsoclonus-myoclonus patients. None of the patients exhibited high levels of monoamine metabolites. Homovanillic acid levels were slightly lower in the cerebrospinal fluid of patients receiving corticotropin or steroids at the time of lumbar puncture. Clinical variables that could be excluded were paraneoplastic etiology, anesthetic for lumbar puncture, syndrome duration, age at onset, gender, response to steroids, length of time until initiation of corticotropin or steroids, presence of seizures, opsoclonus, and functional impairment. These data suggest a disturbance and possible altered ontogeny of serotonin or dopamine neurotransmission in a subpopulation of children with opsoclonus-myoclonus with low cerebrospinal fluid levels of 5-hydroxyindoleacetic acid and homovanillic acid.(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebrospinal fluid 5-hydroxyindoleacetic acid (CSF 5-HIAA) was determined for elderly delirious patients during the acute stage and after a 1-year follow-up period, and the 5-HIAA levels were compared with age-equivalent controls. As compared with the controls, the 5-HIAA levels were significantly higher at the beginning of the index admission in patients with multi-infarct dementia and patients with no apparent CNS disease. The 5-HIAA levels were also higher in the latter subgroup in the 1-year sampling, but no other differences between delirious patients and controls were observed. The one-way procedure showed no differences between the subgroup means of delirious patients when divided according to the severity of cognitive decline or type of delirium in any of the samples. The 5-HIAA levels measured during the index admission correlated with the length of life after delirium suggesting that serotonergic dysfunction may have prognostic significance in delirious patients.
A simple and sensitive method for the simultaneous measurement of 5-hydroxytryptamine and its main metabolite 5-hydroxyindoleacetic acid in rat brain is described. Brain tissue samples were only deproteinated and, without further extraction, were injected directly onto a high-performance liquid chromatography column and detected electrochemically. The detection limit for 5-hydroxytryptamine and 5-hydroxyindoleacetic acid was 16 and 8 g per injection, respectively. Within 8 min, the total separation of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid is achieved. With this method over 100 analyses can be performed in a single working day. Brain samples from young and old, male and female Brown Norway rats were analysed for indoles by this method. The ratio 5-hydroxytryptamine 5-hydroxyindoleacetic acid, an index for serotonin turnover, showed significant differences between age groups and genders in the cortex, and a significant difference between genders in the hypothalamus.
A method has been developed for the separation of 5-hydroxyindoleacetic acid from substances in urine and cerebrospinal fluid which interfere with its fluorometric determination. This involves the use of anion exchange column chromatography with elution of the 5-hydroxyindoleacetic acid by 3 mol/l formic acid in 60% methanol. The indole acid is then assayed fluorometrically after reaction with o-phtalaldehyde. Urinary 5-hydroxyindoleacetic acid values are reported for patients with stable cirrhosis and hepatic encephalopathy and compared with those found in control subjects without liver disease.
The spontaneous release of 5-hydroxytryptamine and its metabolite 5-hydroxyindoleacetic acid from the enterochromaffin cells of the small intestine into the portal circulation was investigated in vitro using the vascularly perfused ileum of the guinea-pig. The release of 5-hydroxytryptamine decreased by 70% in a calcium-free medium and by 35% in the presence of tetrodotoxin. Inhibition of monoamine oxidase activity by pargyline (100 microM) had no effect on the spontaneous release of 5-hydroxytryptamine although it caused a 75% reduction in the outflow of 5-hydroxyindoleacetic acid. Imipramine (1 microM), an inhibitor of neuronal uptake of 5-hydroxytryptamine, reduced the 5-hydroxyindoleacetic acid outflow by 57% and increased the release of 5-hydroxytryptamine by 66%. The combination of both drugs showed no additional effect. The tissue content of 5-hydroxytryptamine and its metabolite was not changed after perfusion with the precursor L-tryptophan or monofluoromethyldopa, an inhibitor of the L-aromatic amino acid decarboxylase. The results show that the spontaneous release of 5-hydroxytryptamine and its metabolite reflects largely calcium-dependent exocytotic release of the amine. "Neuronal uptake" (into aminergic and/or enterochromaffin cells) followed by deamination appears to be the main pathway of 5-hydroxytryptamine catabolism in the guinea-pig ileum.
An HPLC method with electrochemical detection for the simultaneous measurement of serotonin (5-hydroxytryptamine) and 5-hydroxyindoleacetic acid in primary mesencephalic cell culture is described. The serotonin and 5-hydroxyindoleacetic acid cell content was measured on different days of growth in vitro; after twelve days in culture the amounts of serotonin and 5-hydroxyindoleacetic acid detected were 916.0 +/- 70.2 and 215.8 +/- 15.5 pg per well, respectively. The heterogeneity of neurons in our cultures and their capacity to take up serotonin were assessed by measuring the amounts of exogenous serotonin taken up in the presence of different monoamine uptake inhibitors. This method, sensitive and reliable, can represent a valid alternative to the use of labelled compounds.
Cerebrospinal fluid 5-hydroxyindoleacetic acid levels were determined in 31 women with unipolar involutional depression using the probenecid technique. Values were found to be lower in depression as compared to controls, but they did not correlate with the severity of the clinical picture. Anxiety, insomnia and drug response however showed significant correlation with pretreatment 5-HIAA level. Some possible interpretations are discussed.