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Biomedical subjects

P Riederer

Publications and source records attributed to P Riederer.

At least 505 records · Page 28Linked to original sources
PubMed1978

Amphetamine and 2-phenylethylamine in post-mortem Parkinsonian brain after (-)deprenyl administration.

Deprenyl is an inhibitor of monoamine oxidase type B, the enzyme responsible for 2-phenylethylamine oxidation, and is used in conjunction with L-Dopa therapy in Parkinson's disease. Post-mortem studies in human brain tissue have shown that after (-)deprenyl administration to parkinsonian patients amphetamine is present in concentrations up to 56 ng/g. It also could be shown that phenylethylamine concentrations are substantially increased in such patients. Phenylethylamine and amphetamine have been investigated using a gas chromatographic technique.

Amphetamines↗
PubMed1978

Dopamine-sensitive adenylate cyclase activity in the caudate nucleus and adrenal medulla in Parkinson's disease and in liver cirrhosis.

In human caudate nucleus and adrenal medulla dopamine-stimulated adenylate cyclase was measured. At a concentration of 100 microM dopamine, liver cirrhosis, carcinoma and therapy resistent parkinsonian patients showed decreased stimulation or even a reduction compared to controls. Therapy responding parkinsonian patients showed a decreased stimulation compared to controls, but this stimulation was significantly higher than in drug resistent patients.

Adenylyl Cyclases↗
PubMed1978

Human cerebral free amino acids in hepatic coma.

Free amino acids and some related compounds in autopsy specimens of different human brain areas have been determined by column chromatography. Only in patients with hepatic coma could a significant difference in the contents of tyrosine and lysine between caudate nucleus and N. amygdalae be found. In comparison with control subjects the brains of patients with hepatic coma contained significantly higher concentrations of glutamine, isoleucine, histidine and ammonia. In patients with hepatic coma after complete parenteral nutrition plus L-valine administration, dying from other causes, the brain levels of alanine and valine were decreased, while the content of taurine was significantly increased. However, most of the amino acid levels in brain tended toward lower levels. A very significant reduction after treatment with L-valine could be observed in glutamine and ammonia concentration. It is suggested that L-valine has some beneficial action on ammonia detoxification and has also a competing action on amino acid uptake mechanism (specially with the large neutral amino acids).

Adult↗
PubMed1978

Brain monoamines in hepatic encephalopathy and other types of metabolic coma.

Tyrosine (Tyr), tyrosine hydroxylase (TH), tryptophan (Trp), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were assayed spectrofluorometrically and radioenzymatically in various regions of post-mortem brains of human patients with hepatic, uremic, and diabetic coma, liver cirrhosis without coma, and hepatic coma treated with parenteral administration of L-valine, a branched-chain amino acid. The results were as follows: In both hepatic and diabetic coma Tyr was increased as compared to non-comatose cirrhosis and controls, while TH acitivity was within normal limits, indicating sufficient oxygen supply of the brain in both types of coma. Brain DA showed a mild decrease in all types of metabolic coma. Brain Trp was not considerably changed in non-comatose cases of liver cirrhosis and after L-valine treatment of hepatic encephalopathy, but was significantly increased in hepatic coma, with highest elevation in the brainstem tegmentum. Both 5-HT and 5-HIAA were not significantly changed in non-comatose cirrhosis, while a general increase with prevalence for the brainstem was obvious in all types of metabolic coma. After L-valine treatment of hepatic coma, 5-HT levels were usually decreased below control values, while 5-HIAA levels were at or below controls. These results in human post-mortem brains confirm previous CSF and brain findings in experimental and human hepatic and uremic encephalopathies, indicating derangement of brain monoamine neurotransmitter metabolism which is attributed to imbalance of aromatic and branched-chain amino acids in plasma and brain. Increased cerebral 5-HT turnover, particularly in the ascending serotonergic brainstem systems, due to derangement of brain uptake of Trp is suggested to represent an important biochemical substrate of disorders of consciousness in hepatic failure and other types of metabolic encephalopathies. Clinical improvement of hepatic encephalopathy and of the underlying neurotransmitter derangements by administration of L-valine and the possible role of this competitive amino acid on intermediary metabolism and ammonia detoxification are discussed.

Aged↗
PubMed1978

CNS Modulation of adrenal tyrosine hydroxylase in Parkinson's disease and metabolic encephalopathies.

Tyrosine hydroxylase (TH) activity was assayed radioenzymatically in various regions of post-mortem brains of human individuals without neurologic disorders (controls), with Parkinson's disease, senile dementia, hypertensive encephalopathy, hepatic and diabetic coma, liver cirrhosis without coma, and hepatic coma treated with parenteral administration of L-valine. In addition TH activity of the post-mortem adrenal medulla was assayed in controls, in Parkinson's disease, senile dementia and hypertensive encephalopathy. In Parkinson's disease TH activity was significantly decreased in the nigrostriatal system, and less severe in other brainstem areas, while the raphé-reticular formation and limbic system showed normal values. In addition, there was significant decrease in the TH activity of the adrenal medulla, suggesting that Parkinson's disease is a generalized disorder not limited to distinct CNS areas, and that impairment of the dopaminergic niggro-striatal system may involve the TH activity in the adrenal medulla, thus inducing disorders of the peripheral sympathetic system. Senile brain atrophy showed no definite changes in brain, except the striatum, and adrenomedullary TH, while in one case of hypertensive encephalopathy due to long-term corticosteroid treatment normal TH activity in the adrenal medulla was opposed by decreased striatal TH activity, probably due to cerebral ischemia. TH activity in the caudate nucleus of individuals with both hepatic and diabetic coma were within normal ranges, suggesting a sufficient energy supply of the brain during such metabolic catastrophes, while reduced brain TH activity in patients with hepatic coma who died of acute gastrointestinal bleeding is probably due to severe final cerebral ischemia. No correlative data on brain and adrenomedullary TH activities in metabolic encephalopathies are available so far.

Aged↗
PubMed1978

Changes of some putative neurotransmitters in human cerebral infarction.

Dopamine (DA), serotonin (5-HT), tryptophan (TRP), 5-hydroxyindole acetic acid (5-HIAA), and GABA were assayed spectrofluorometrically in various regions of 16 human post-mortem brains with acute and old cerebral infarction. In both recent and older strokes a total depletion of DA and 5-HT in the necrotic tissue was associated with mild reduction of these compounds in remote non-ischemic areas of the injured, and less of the contralateral cerebral hemispheres. 5-HIAA was significantly reduced in acute ischemic necrosis, while the perifocal edema zone showed considerable accumulation of both 5-HT and 5-HIAA. Marked elevation of the 5-HT precursor TRP and of GABA was present in both the necrotic center and perifocal edema of acute infarcts, which also showed a mild reduction of total proteins. The degradation zone surrounding old infarcts showed a mild decrease of both 5-HT and 5-HIAA with normal TRP levels, indicating normalization of the previously increased 5-HT metabolism and turnover after decrease of acute cerebral edema. These data which confirm previous studies in experimental cerebral ischemia and stroke indicate that disorders in the metabolism of brain monoamines and other putative neurotransmitters contribute to the development of postischemic brain damage and the complicating cerebral edema. They are also in keeping with the concept that unilateral focal ischemia produces bilateral effects on brain monoamines.

Aged↗
PubMed1977

Implications of combined treatment with 'Madopar' and L-deprenil in Parkinson's disease. A long-term study.

In a clinical trial the effect of L-deprenil, a selective irreversible inhibitor of monoamine oxidase (M.A.O.) "type B" in potentiating the anti-kinetic properties of levodopa has been investigated in 223 patients. Both drugs were given orally, levodopa as 'Madopar' (levodopa plus the peripherally acting decarboxylase inhibitor, benserazide) 250 mg three times daily and L-deprenil 5 mg once or twice daily. The addition of L-deprenil to madopar therapy resulted in a statistically significant (P less than 0-01-0-001) reduction in patients' functional disability on average within 60 min after a single oral dose and lasting for 1 to 3 days. Dyskinesia occurred in 16 patients, psychosis in 14, orthostatic hypotension in 5, and nausea in 8. Reduction of the L-deprenil dose to 5 mg in these patients eliminated some of the side-effects. Two-thirds of the patients with side-effects had suffered from parkinsonism for between 7 and 15 years. 14% of the patients failed to respond to madopar-deprenil therapy. It is suggested that L-deprenil may act through inhibition of brain M.A.O. as well as by a psychostimulant effect similar to that of amphetamine which occurs through the release of dopamine. Both mechanisms would make more dopamine available at dopamine receptor sites.

Administration, Oral↗
PubMed1977

Brain-noradrenaline and 3-methoxy-4-hydroxyphenylglycol in Parkinson's syndrome.

1. Significantly reduced values of noradrenaline in Parkinson's disease were observable in all brain areas which were studied. 2. A topographic distribution of free 3-methoxy-4-hydroxyphenylglycol (MHPG) can be demonstrated in the human brain. As MHPG in the various brain areas shows a different pattern of concentration it seems that this metabolite of noradrenaline is of physiological significance and is able to reflect noradrenaline turnover. The highest values of free MHPG were found in the hypothalamus, n. accumbens, thalamus and n. ruber. 3. In a limited series of patients with Parkinson's disease post mortem analysis indicated lower values of MHPG in caudate n., putamen, s. nigra, red nucleus and n. accumbens. All other brain areas did not show significant alterations. 4. Parkinsonian patients who died during Madopar therapy demonstrated a significant increase of MHPG in caudate n., putamen, s. nigra, n. ruber, n. amygdalae and n. accumbens when compared to the untreated group, indicating an enhanced turnover of noradrenaline in these areas. 5. Bound MHPG has been estimated in various brain areas as to be in the range of 13--38 percent of free MHPG.

Brain Chemistry↗
PubMed1977

Brain monoamines in metabolic (endotoxic) coma. A preliminary biochemical study in human postmortem material.

Spectrofluorometric assays of DA, 5-HT and 5-HIAA were performed in different areas of postmortem brains of humans who died in hepatic and uremic coma. Brain DA showed a mild general decrease, the average reduction being 20 to 30 percent of the controls. By contrast, 5-HT and 5-HIAA were markedly increased in most brain areas, most significantly in the reticular and raphé nuclei of the brainstem and in some parts of the limbic system. Despite individual and regional differences, the monoamine changes had similar patterns in both hepatic and uremic coma. These data in human brain which confirm previous clinical and experimental studies in hepatic encephalopathy suggest some common disorders of central monoamine metabolism in endotoxic coma of different origin. Brain edema, a constant feature in toxic coma, is probably due to increased 5-HT content in the brain, the pathophysiologic effect of 5-HT on the blood-brain barrier being well established. The prominent changes of indoleamine metabolism in the reticular brainstem and limbic systems may be related to disorders of consciousness.

Aged↗
PubMed1977

Electrophoresis of unconcentrated natural cerebrospinal fluid.

A rapid and simple method to perform protein electrophoresis for natural unconcentrated cerebrospinal fluid is described. Hereby, pherograms with technically incontestable separations are acquired with a running time of 70 min at 180 V.

Cerebrospinal Fluid Proteins↗
PubMed1976

Time course of nigrostriatal degeneration in parkinson's disease. A detailed study of influential factors in human brain amine analysis.

It could be shown that the post mortem analysis of biogenic amines, precursors and metabolites in the human brain are influenced by various parameters. 1. The patient's medical history; long term observations of the course of the disease; age; sex. 2. Terminal illness; duration of terminal illness. 3. Previous treatment with drugs; last drugs. 4. Time interval between last drug treatment and death; time of day and date of last drug consumption. 5. Rapidity of death; time of death; duration of coma. 6. Changes occurring in tissues before death; patients' constitution during terminal illness. 7. Changes in concentration of the biogenic amines, precursors, and metabolites depending on the patient's age. 8. Time between death and necropsy. 9 Dissection of specimen. 10. Period of storage; temperature of storage. 11. Chronbiological rhythm of substances. 12. Methods of assayL 13. Homogeneity of all mentioned parameters in the control group and patient's group. For the first time it could be demonstrated that the time course of nigrostriatal degeneration, independent of the age of the parkinsonian at the beginning of the illness, is linear for the last stage and the denervation progressively increases as the duration of illness progresses.

Age Factors↗
PubMed1976

Serotonin, noradrenaline, dopamine metabolites in transcendental meditation-technique.

The highly significant increase of 5-HIAA (5-hydroxyindole-3-acetic acid) in Transcendental Meditation technique suggests systemic serotonin as "rest and fulfillment hormone" of deactivation-relaxation. Furthermore 5-HT (5-hydroxytryptamine, serotonin) is considered to be the EC-cell (enterochromaffine-cell) hormone requested by Fujita and Kobayashi and its role for EEG synchronisation via area postrema chemoreceptor as anti arousal agent is being discussed. The significant decrease of the catecholamine metabolite VMA (vanillic-mandelic acid) in meditators, that is associated with a reciprocal increase of 5-HIAA supports as a feedback necessity the "rest and fulfillment response" versus "fight and flight". As the adreno medullary tissue serves for hormonal reinforcement of orthosympathetic activity, the Enterochromaffine Cell System (having taken the form of distinct organs in some species as octopus and discoglossus) is suggested to serve via serotonin for humoral reinforcement of parasympathetic activity in deep relaxation.

Adult↗