Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypotensive drug alphamethyldopa, an inhibitor of serotonin synthesis, caused significant hypothermia ranging from 33.4 to 34.8 degrees C (t=3.09 at P less than 0.05) in four out of nine hypertensive patients, with evidence of cerebral atherosclerosis. The anti-serotonin effect of alphamethyldopa correlated with statistically significant (t=6.8 at P less than 0.001) fall in the 24 hour urinary 5-hydroxyindoleacetic acid on the third day of the therapy. The possible mode of hypothermic side effect is discussed.
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PMID:Hypothermia dn alphamethyldopa treatment. 101 Jun 37

Repeated treatment with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) resulted in significant attenuation of 8-OH-DPAT-induced hypothermia and adrenocorticol effect in mice of both sexes, while it did not affect the 8-OH-DPAT-induced decrease in 5-hydroxyindoleacetic acid in the hypothalamus in either sex. The attenuated responses developed more rapidly in female than in male mice, indicating sex differences in the adaptive regulation of the 5-HT1A receptor-mediated responses.
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PMID:Sex difference for tolerance of 5-HT1A receptor-mediated temperature and corticosterone responses in mice. 138 74

In previous studies we documented an increase in the levels of the serotonin metabolite, 5-hydroxyindoleacetic acid, in the congenitally hyperammonemic sparse fur mouse. To extend these findings, brain serotonin receptors were studied in these animals. Radioligand binding assays were performed using [3H]ketanserin to label serotonin2 sites and 8-[3H]hydroxy(di-n-propylamino)tetralin to label serotonin1A sites in cortical membrane homogenates. The capacity (Bmax) for [3H]ketanserin binding was significantly lower (-21%; p less than 0.05) in sparse fur animals than in control animals; there was no change in affinity (KD). In contrast, the capacity for 8-[3H]hydroxy(di-n-propylamino)tetralin binding was significantly greater (26%; p less than 0.05) in sparse fur compared with control animals. No difference in affinity was observed. Using two behavioral assays, the functional responsiveness of these serotonin receptors was compared in sparse fur and control animals. Head twitch activity elicited by administration of the serotonin agonist quipazine was studied as a behavior mediated by serotonin2 receptors. Compared with controls, sparse fur mice demonstrated a significantly decreased head twitch response (p less than 0.005). Hypothermia elicited by administration of 8-hydroxy(di-n-propylamino)tetralin was studied as a physiologic response mediated by serotonin1A receptors. Although there were not overall group differences in the dose-response data, there was a significant increase in the hypothermia induced by 8-hydroxy(di-n-propylamino)tetralin in sparse fur compared with control mice (p less than 0.02) at the highest dose. These data provide further support for a link between hyperammonemia and alterations in the serotonin system.
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PMID:Brain serotonin2 and serotonin1A receptors are altered in the congenitally hyperammonemic sparse fur mouse. 153 55

A study was conducted to investigate changes in monoamine metabolism in the brain of rats with acute ischemic hepatic failure (AHF) induced by two-stage hepatic devascularization. Strict artificial cardiopulmonary management was used to exclude possible confounding effects of hypotension, hypothermia and hypoxemia that often appear in AHF. Rats were put in an incubator at 34 degrees C before the ligation of the hepatic artery (second stage operation), tracheotomized and ventilated artificially throughout the remaining experimental periods. No significant difference was observed in physiological parameters, including body temperature, pulse rate and systolic arterial blood pressure or PaO2 between AHF and sham operated rats. Brain levels of norepinephrine (NE) and its metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG), dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanilic acid (HVA), and serotonin (5-hydroxytryptamine, 5HT) and its metabolite 5-hydroxyindoleacetic acid (5HIAA) were determined by HPLC-voltametry. AHF rats showed significantly higher MHPG, DOPAC, 5HIAA and lower NE levels in the brain compared to controls. In addition, a significant negative correlation between NE and tyrosine (Tyr), a significant positive correlation between MHPG and Tyr or phenylalanine (Phe), and a significant positive correlation between DOPAC and Tyr or Phe were observed. In conclusion, the changes in monoamine metabolism in the brain of AHF rats are clearly induced specifically by hepatic failure itself, possibly through an altered metabolism of amino acids.
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PMID:Changes in brain monoamine metabolism in rats with acute ischemic hepatic failure under artificial cardiopulmonary management. 157 24

The effects of repeated treatment of rats with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), 1.0 mg/kg, subcutaneously, twice daily for 7 days, on the stimulation of post- and presynaptic 5-HT1A receptors were examined. The postsynaptic responses, hypothermia and inhibition of the cage-leaving response, evoked by 0.05 mg/kg 8-OH-DPAT, were measured 48 hr after the final injection. Another postsynaptic response, the 5-HT syndrome (flat body posture and forepaw treading) was observed after the third injection of 8-OH-DPAT (1.0 mg/kg s.c.). One presynaptic response examined was the 8-OH-DPAT-induced decrease in the concentration of 5-hydroxyindoleacetic acid (5-HIAA), that indicates a decrease in turnover of 5-HT, due to stimulation of 5-HT receptors on the cell bodies and measured as the ratio of 5-HIAA to 5-HT in the hippocampus, hypothalamus and medulla oblongata. Another presynaptic response was the 8-OH-DPAT-induced decrease in the accumulation of 5-hydroxytryptophan (5-HTP) in the hippocampus and hypothalamus, after inhibition of L-aromatic amino acid decarboxylase by 3-hydroxybenzylhydrazine (NSD 1015), that is due to stimulation of autoreceptors on the 5-HT cell bodies. The kinetic properties of 5-HT1A receptors in the cerebral cortex and hippocampus, hippocampus alone, hypothalamus and medulla oblongata were determined with [3H]8-OH-DPAT. It was found that the postsynaptic effects were markedly attenuated after the treatment, the hypothermic effect already after a single dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Different effects on the responses of functional pre- and postsynaptic 5-HT1A receptors by repeated treatment of rats with the 5-HT1A receptor agonist 8-OH-DPAT. 169 32

The effects of the tryptamine metabolite, indoleacetic acid (IAA) on body temperature and serotonin (5-HT) metabolism in mice were investigated. IAA at 300 mg/kg i.p. induced significant hypothermia in mice. It caused a remarkable decrease in concentration of total tryptophan (TRP) and a considerable increase in free TRP in serum. IAA increased 5-HT, 5-hydroxyindoleacetic acid and TRP in the brain, but decreased 5-HT synthesis in the brain. The 5-HT antagonist, methysergide and the 5-HT depleter, p-chlorophenylalanine did not affect IAA-induced hypothermia.
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PMID:Indoleacetic acid-induced hypothermia and changes in serotonin metabolism in mice. 241 96

Serotonin and 5-hydroxyindoleacetic acid levels were measured in the brains of mice following intraperitoneal administration of 10 mg/kg p-chloramphetamine (PCA). Indolyl levels were decreased at the 60 min interval, but were unchanged 30 min following PCA injection. PCA-induced hypothermia was found to be dependent upon dose and ambient temperature. Hypothermia was attenuated by cyproheptadine and slightly enhanced in the presence of fluoxetine. Mechanisms other than intraneuronal release and serotonin depletion appear to mediate PCA-induced hypothermia.
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PMID:Cyproheptadine antagonism of p-chloroamphetamine hypothermia in mice. 242 48

Changes in catecholamines (CA) in the plasma and urine and metabolites of CA and serotonin (5-HT) in the cerebrospinal fluid of guinea-pigs in hypothermia (Trec 30 degrees C) and after subsequent rewarming were determined with HPLC in order to obtain data on early stress reactions and their timing. Both noradrenaline (NA) and adrenaline (A) were low in the plasma but high in the urine after the hypothermic period. These had normalized in the plasma after rewarming but were still high in the urine. Dopamine values tended to be low (not significant). Methoxyhydroxyphenylglycol and homovanilic acid were elevated in the cerebrospinal fluid both after hypothermia and following rewarming, and 5-hydroxyindoleacetic acid after rewarming. The ratio of adrenaline to noradrenaline, the catecholamine hypothermia index, in the urine had risen 24-fold after hypothermia and 40-fold after rewarming. The results support the view that elevated catecholamine concentrations in the urine and elevated values of their metabolites in the cerebrospinal fluid could be regarded as hypothermia markers. However, other stress conditions, which have lasted at least a few hours, should be excluded in the final interpretation.
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PMID:Plasma and urine catecholamines and cerebrospinal fluid amine metabolites as hypothermia markers in guinea-pigs. 274 75

Guinea-pigs were treated with chlorpromazine or 0.9% NaCl and exposed to +4 degrees C or +23 degrees C for 2 h. Hypothalamic noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT), 3-methoxy-4-hydroxyphenylethylene-glycol (MHPG), homovanillinic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were determined by high-performance liquid chromatography. Serum and urinary catecholamines, muscle and liver glycogen and blood glucose were also measured. Chlorpromazine caused deep hypothermia at this moderately cold temperature and slight hypothermia at room temperature. Cold increased the activity of noradrenergic and serotonergic neurons, as indicated by the increase in hypothalamic MHPG and 5-HIAA and also the MHPG:NA and 5-HIAA:5-HT ratios. A tendency towards drug-induced inhibition of hypothalamic serotonergic neurons was seen, although this was not significant. A drug-induced inhibition of noradrenergic neurons could not be ruled out. Increased drug-induced turnover of DA was observed in the cold, and a tendency in the same direction was seen at room temperature. Excretion of DA into the urine was induced by chlorpromazine. The hypothermic guinea-pigs had low serum catecholamines, indicating diminished sympathetic activity, but high urinary catechols, a sign of cold stress.
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PMID:Effects of chlorpromazine on hypothalamic aminergic neurons and stress responses in moderate cold. 275 78

To characterize the transport system of cimetidine, an organic cation, in the blood-cerebrospinal fluid barrier, the accumulation of cimetidine by the isolated rat choroid plexus was examined. Accumulation of cimetidine was against a concentration gradient via a saturable process (Km = 53 microM, Vmax = 12 nmol/ml/min) that was inhibited by sulfhydryl reagents (p-hydroxymercuribenzoate), metabolic inhibitors (KCN and 2,4-dinitrophenol) and hypothermia (Q10 = 4.5), but did not require inward Na+ gradient. Organic cations such as 1N-methylnicotinamide, tetraethylammonium, choline, histamine and creatinine did not affect the accumulation of cimetidine at the concentration of 1 mM. Cimetidine did not affect the accumulation of tetraethylammonium. More lipophilic cations such as quinidine and quinine inhibited not only the accumulation of cimetidine but also that of an organic anion, benzylpenicillin, although the inhibitory mechanisms are not known. One millimolar of organic anions, such as 5-hydroxyindoleacetic acid, p-aminohippuric acid, homovanillic acid, salicylic acid and benzylpenicillin, inhibited the accumulation of cimetidine. Furthermore, the accumulation of organic anions (benzylpenicillin and salicylic acid) showed saturability and was inhibited by cimetidine. Cimetidine and the organic anions thus showed a mutual inhibition. Oligopeptides also inhibited the accumulation of cimetidine. These findings suggested that cimetidine transport in the choroid plexus is via carrier-mediated active transport process, but does not require inward Na+ gradient. This transport is inhibited by several compounds with different properties like oligopeptides, lipophilic cations and organic anions, although the inhibitory mechanism is not known.
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PMID:Transport of cimetidine by the rat choroid plexus in vitro. 379 52


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