homovanillic acid/beroerte

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Values of vanillylmandelic acid and homovanillic acid in the urine as potential prognostic biomarkers in ischaemic stroke patients.

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BACKGROUND Suitable biomarkers that have prognostic values are one of the key points of interest in ischaemic stroke. Increased sympathetic nervous system activity in ischaemic stroke causes multiple local and systemic effects that can be detrimental to the outcome. The mechanism of action is

Homovanillic acid and 5-hydroxyindoleacetic acid modifications in CSF of patients with stroke and multi-infarct dementia.

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Thirty four patients who had complete ischemic stroke confirmed by neurologic examination, were divided into three groups according to the time elapsed between the first signs of stroke and lumbar puncture: group A, 22-47 h; group B, 48-71 h; group C, 72-96 h. Nineteen patients with multi-infarct

[The changes of monoamine metabolites in CSF of patients with cerebral stroke].

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For understanding of the role of monoamines in cerebral ischemia, 3-methoxy-4-hydroxyphenylglycol (MHPG), hydroxyindoleacetic acid (5HIAA) homovanillic acid (HVA) the three major monoamine metabolites in CSF of 33 patients and 18 controls were measured with high-performance liquid chromatography.

Different patterns of CSF neurotransmitter metabolism in patients with left or right hemispheric stroke.

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In 30 ischemic stroke patients, divided into 2 groups depending on the side of their hemispheric cerebral lesion, the authors evaluated the levels of CSF homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA). The changes of these metabolites in CSF samples collected 3, 14 and 25 days after

Increased monoamine metabolite concentrations and cholinesterase activities in cerebrospinal fluid of patients with acute stroke.

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Twenty-one patients with acute brain infarction, 8 with transient ischemic attack and 20 controls were investigated for lumbar cerebrospinal fluid (CSF) monoamine metabolites and cholinesterases. The diseased patients were lumbar punctured on 2 occasions, mean Days 1 (0-3) and 5 (3-9) after debut of

Excitatory amino acids and monoaminergic neurotransmitters in cerebrospinal fluid of acute ischemic stroke patients.

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OBJECTIVE Improved insight in the role of neurotransmitters in acute cerebral ischemic injury may be fundamental for the successful development of novel therapeutic approaches. We investigated excitatory amino acids and monoaminergic neurotransmitters in cerebrospinal fluid (CSF) of acute ischemic

Neuroanatomic pathways associated with monoaminergic dysregulation after stroke.

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We examined the complex relationship between lesion location, symptoms of depression (affective and apathetic), and monoamine dysfunction after stroke. Magnetic resonance imaging was performed on 48 post-stroke patients that had been assessed for affective and apathetic symptoms using the Hospital

Amine metabolites in ventricular cerebrospinal fluid in coma.

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The concentrations of homovanillic acid (HVA), 3-methoxy, 4-hydroxyphenylglycol (MHPG), and 5-hydroxyindolylacetic acid (5-HIAA) were measured in samples of ventricular cerebrospinal fluid (CSF) taken from 15 patients who were comatose as a result of an acute head injury, a tumour, or a

Monoamine metabolites in cerebrospinal fluid during acute cerebral ischemia.

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To clarify the rule of monoamine in cerebral ischemia, 3-methoxy-4-hydroxyphenylglycol (MHPG), 5-hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) in cerebrospinal fluid (CSF) of 33 patients and 18 controls were measured with high performance liquid chromatography. Results showed all the

Plasma monoaminergic metabolites and catecholamines in subarachnoid hemorrhage. Clinical implications.

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We examined plasma catecholamines and monoaminergic metabolites (3-methoxy-4-hydroxyphenylethyleneglycol [MHPG], homovanillic acid [HVA], and 5-hydroxyindoleacetic acid) in patients with stroke successively up to three weeks after the initiation of symptoms. Plasma levels of free catecholamines were

Monoamine metabolites in cerebrospinal fluid during and after acute cerebral ischemia.

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In order to understand the role of monoamines in cerebral ischemia, 3-methoxy-4-hydroxyphenylglycol(MHPG), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid(HVA), the three major unconjugated monoamine metabolites in cerebrospinal fluid (CSF), of 33 patients and 18 controls were measured

Lateralized effect of cerebral infarction on spinal fluid monoamine metabolite concentrations in rats.

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Using a rat model of stroke, we studied the effect of unilateral middle cerebral artery ligation on cerebrospinal fluid monoamine metabolites at different intervals over a 40-day postoperative period. Male Sprague-Dawley rats were divided into four groups: an unoperated control group (n = 9), a

[Effects of gamma-hydroxybutyrate on monoamine metabolism and protein synthesis after transient global cerebral ischemia].

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The effects of gamma-hydroxybutyrate (GHB) on 1) monoamine metabolism, and 2) protein synthesis were examined in a gerbil stroke model. The monoamine metabolism was studied by occluding bilateral common carotid arteries for 15 minutes followed by GHB administered intravenously 3 hours later. Tissue

Metabolism of monoamine neurotransmitters in the evolution of infarction in ischemic striatum.

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The time course of changes in monoamine metabolism in ischemic striatum was assessed by measurement of levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT) and 5-hydroxy-indole-acetic acid (5-HIAA) 2, 4, 7 and 16 hours after irreversible unilateral

Site-specific activation of dopamine and serotonin transmission by aniracetam in the mesocorticolimbic pathway of rats.

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The effects of aniracetam on extracellular levels of dopamine (DA), serotonin (5-HT) and their metabolites were examined in five brain regions in freely moving stroke-prone spontaneously hypertensive rats (SHRSP) using in vivo microdialysis. Basal DA release in SHRSP was uniformly lower in all

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