3 4 dihydroxyphenylacetic acid/hypoxie

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Hypoxia during early developmental period induces long-term changes in the dopamine content and release in a mesencephalic cell culture.

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The present study was conducted to elucidate the long-term effects of exposure to hypoxia of dopaminergic neurons during the early developmental period. Primary mesencephalic cell cultures prepared from fetal rats and containing 0.5-2% of dopaminergic neurons were exposed to hypoxia between in vitro

[Effect of S-adenosyl-L-methionine on cerebral monoamine turnover after hypoxia in rats].

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The effects of S-Adenosyl-L-methionine (SAMe) on cerebral monoamine turnover at 60 min of reoxygenation after hypoxia (PaO2, 31-35 mmHg) for 15 min were studied in 44 rats anesthetized with nitrous oxide. The accumulations of monoamine metabolites: 3-methoxy 4-hydroxyphenylglycol (MHPG),

[Long-term effects of postnatal hypoxia on monoamine and amino acid levels in the rat brain].

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Perinatal hypoxia is known as a risk factor for human epilepsies. Previous studies in our laboratory have shown that the rats with postnatal hypoxia show facilitation of the kindling formation and enhanced susceptibility to pentylenetetrazol (PTZ)-induced seizures even after the maturation. In the

Monoamine neurotransmitter metabolism and locomotor activity during chemical hypoxia.

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The effects of hypoxia on metabolism of 5-hydroxytryptamine (5-HT or serotonin) and 3,4-dihydroxyphenylethylamine (DA or dopamine) were compared with those on open-field activity in male CD-1 mice. Chemical hypoxia was induced with NaNO2. Hypoxia did not alter striatal concentrations of DA, 5HT,

Free and conjugated catecholamines and metabolites in cat urine after hypoxia.

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Catecholamine and metabolite excretion was studied in the cat after 6 h of 7.5% O2 hypoxia. Norepinephrine (NE) release from sympathetic nervous endings was strongly activated, whereas epinephrine (E) excretion was only slightly increased. A noteworthy result was the increase of dopamine (DA) and

Resveratrol protects rat striatal slices against anoxia-induced dopamine release.

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Incubation of rat striatal slices in anoxic medium caused significant alterations in dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) outputs; while DA release increased several times, 50% decline in DOPAC output was observed under this condition. Tissue ATP level, on the other hand, was

Effect of anoxia on striatal monoamine metabolism in immature rat brain compared with that of hypoxia: an in vivo microdialysis study.

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We examined in 5-day-old rats the effects of either anoxia or 8% hypoxia on extracellular monoamines such as dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), norepinephrine (NE), 5-hydroxytryptamine (5-HT), and 5-hydroxyindole-3-acetic acid (5-HIAA) using in vivo

Assessment of fatigue-related biochemical alterations in a rat swimming model under hypoxia.

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It is well known that exercise-induced fatigue is exacerbated following hypoxia exposure and may arise from central and/or peripheral mechanisms. To assess the relative contribution of peripheral and central factors to exercise-induced fatigue under hypoxia, a rat model of fatigue by a bout of

Hypoxia induces differential changes of dopamine metabolism in mature and immature mesencephalic and diencephalic cell cultures.

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Perinatal hypoxia is known as a high risk factor for the development of long-lasting abnormalities in dopaminergic system. The early developmental alterations of dopamine (DA) metabolism induced by hypoxia could contribute to these abnormalities. To understand the hypoxia-induced changes of intra-

The regulation of dopamine and noradrenaline in the rat carotid body and its modification by denervation and by hypoxia.

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1. The mechanism whereby hypoxia lasting 20 min elicits a decrease in the dopamine content of rat carotid bodies was studied. 2. The concentrations of dopamine, noradrenaline, dihydroxyphenylacetic acid and homovanillic acid in carotid body were measured by a mass-fragmentographic procedure. The

Dopamine and norepinephrine dynamics in rat carotid body during long-term hypoxia.

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The contents of dopamine (DA), norepinephrine (NE) and 3,4-dihydroxyphenylacetic acid (DOPAC), and the utilization rates (secretion plus breakdown) of DA and NE were measured in carotid bodies of rats exposed, to normobaric hypoxia (10% O2 + 90% N2) for 0, 2, 7, 14 or 28 days. Long-term hypoxia

Long-term hypoxia increases the turnover of dopamine but not norepinephrine in rat sympathetic ganglia.

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The content and turnover of dopamine, 3,4-dihydroxyphenylacetic acid and norepinephrine have been investigated in the superior cervical, coeliac and mesenteric ganglia of rats exposed to moderate normobaric hypoxia (10% O2 in N2) lasting for 2-28 days. the turnover was estimated by the decrease in

Magnesium attenuates a striatal dopamine increase induced by anoxia in the neonatal rat brain: an in vivo microdialysis study.

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We evaluated the effects of magnesium on extracellular dopamine (DA) and its metabolites in the striatum of 5-d-old rats submitted to 16 min of anoxia using microdialysis and HPLC. Rat pups were divided into three groups and received either 1) intrastriatal perfusion (IS) of MgSO4, 2)

Prenatal cocaine exposure and postnatal hypoxia independently decrease carotid body dopamine in neonatal rats.

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The effects of prenatal cocaine exposure on the levels of carotid body dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were investigated in 5-day-old rat pups exposed to normoxic and hypoxic conditions. Timed-pregnant Sprague-Dawley rats were

Anoxia-induced dopamine release from rat striatal slices: involvement of reverse transport mechanism.

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Incubation of rat striatal slices in the absence of oxygen (anoxia), glucose (aglycemia), or oxygen plus glucose (ischemia) caused significant increases in dopamine (DA) release. Whereas anoxia decreased extracellular 3,4-dihydroxyphenylacetic acid levels by 50%, aglycemia doubled it, and ischemia

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