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homovanillic acid/otok

Веза се чува у привремену меморију
11 резултати

Renal excretion of vanillylmandelic acid and homovanillic acid in rats with paw edema or adjuvant arthritis.

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1. Urinary excretion of unconjugated vanillylmandelic acid (VMA) and homovanillic acid (HVA) was found to be decreased in adjuvant arthritic rats. The decrease is apparently not due to impaired animal activity, but it could be explained by the reduction of catecholamine biosynthesis and/or release

Experimental quantitative evaluation of transvascular removal of unnecessary substances in brain edema fluid.

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We developed a model by which the transvascular removal of unnecessary substances in brain edema fluid could be measured quantitatively and chronologically. Brain stab wounds were produced in Wistar rats by insertion of paired microdialysis probes in the unilateral caudatoputamen. Homovanillic acid

Homovanillic acid and 5-hydroxyindole-acetic acid in the csf of patients after a severe head injury. II. Ventricular csf concentrations in acute brain post-traumatic syndromes.

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Ventricular concentrations of homovanillic acid (HVA) and 5-hydroxyindole-acetic acid (5HIAA) were measured in 7 patients a few days after a severe traumatic brain injury. Both acid metabolites were elevated in respect to control patients values, however, the rise was more consistent for 5HIAA (258

Hormonal correlates of the inadequate natriuretic response to salt loading in idiopathic edema.

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The purpose of this study was to evaluate the body fluid and hormonal responses to salt loading in patients with idiopathic edema. In response to a combined intravenous and oral salt loading, patients with idiopathic edema were found, compared to control women, to have more weight gain, an increase

Effect of dexamethasone on monoamine and metabolite levels in a brain-tumor model.

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Neurological improvement in brain-tumor patients treated with dexamethasone (DEX) precedes a reduction in peritumor brain edema. In the study reported here, levels of noradrenaline (NA), dopamine (DA) and 5-hydroxytryptamine (5-HT), homovanillic acid (HVA) and 5-hydroxyindole-3-acetic acid (5-HIAA)

Effects of postnatal trimethyltin or triethyltin treatment on CNS catecholamine, GABA, and acetylcholine systems in the rat.

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The effects on brain neurochemistry of two neurotoxic tin compounds, trimethyltin (TMT) hydroxide and triethyltin (TET) sulfate, were examined. Long-Evans rats were treated with TMT hydroxide (1 mg/kg, i.p.) on alternate days from day 2 to 29 of life. These treatments caused a weight deficit of

Effect of MCI-186 on ischemia-induced changes in monoamine metabolism in rat brain.

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We examined the effects of MCI-186 (3-methyl-1-phenyl-2-pyrazolin-5-one), a novel free radical scavenger and an inhibitor of ischemia-induced brain edema, on monoamine metabolism in the brains of both normal and ischemic rats. In normal rats, 3 mg/kg i.v. MCI-186, a dose that prevents ischemic brain

L-646,462, a cyproheptadine-related antagonist of dopamine and serotonin with selectivity for peripheral systems.

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The selectivity, peripheral vs. central actions, of the antidopaminergic agent L-646,462 was assessed in two ways. First, elevation of prolactin in serum (peripheral) and homovanillic acid in the striatum were measured in rats. L-646,462 was found to have a central/peripheral activity ratio of 143,

Aminergic neurotransmitter and water content changes in rats after transient forebrain ischemia.

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We have studied changes of cerebral monoamine metabolism and water content, during recirculation following global transient ischemia (20 min) using the four-vessel occlusion model in rats. Levels of monoamines and their metabolites were determined in cortex, striatum, hippocampus, and hypothalamus.

The acute histopathology of MPTP in the mouse CNS.

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We found that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) rapidly induced cytopathological changes in the brain, involving some neurons selectively, as well as astrocytes and blood vessels. Dopaminergic neurons in the midbrain, as identified by immunostaining for tyrosine hydroxylase, were

Kainic acid induced seizures: neurochemical and histopathological changes.

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Behavioural, histopathological and neurochemical changes induced by systemic injection of kainic acid (10 mg/kg, s.c.) were investigated in rats. The most pronounced behavioural changes were strong immobility ("catatonia"), increased incidence of "wet dog shakes", and long-lasting generalized
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