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)

Dopamine (DA) was injected in the third brain ventricle of goats and the thermoregulatory effects were studied under different ambient conditions. The effects depended on dose, ambient conditions and cannula used. In the cold, there was a drop in body temperature, sometimes accompanied by suppression of shivering and by vasodilatation. Both temperature decrease and suppression of shivering were dose-dependent but there was no relation between magnitude of temperature drop and occurrence of shivering suppression. In a thermoneutral environment, there was either a slight vasoconstriction or hypothermia, occasionally accompanied by induction of panting. In the heat, either hypothermia or hyperthermia was observed. Hypothermia was accompanied by an increase in panting. Hyperthermia only occurred when the animals became excited as a result of the injection of DA. It is concluded that DA acts by stimulating the thermoregulatory pathway from heat sensors to heat loss effectors at a locus similar to that for 5-hydroxytryptamine in the thermoregulation model of Bligh et al. (1971).
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PMID:Thermoregulatory effects of intraventricularly injected dopamine in the goat. 86 60

1. The effect of various agents injected into the cerebral ventricles of the mouse, upon the tremor and hypothermia produced by oxotremorine (0.5 mg/kg i.p.) was studied. 2. Acetylcholine (0.1-10 mug) produced a dose-dependent potentiation of oxotremorine tremor in contrast to the multiphasic effect it had on the accompanying hypothermia. Both tremor and hypothermia were antagonised by very small doses (0.1-10 ng) of atropine. 3. Dopamine and apomorphine (0.1-10 mug) had no significant effect on oxotremorine tremor. A dose-dependent potentiation of hypothermia was, however, observed. 4. Noradrenaline (0.1-10 mug), phentolamine and propranolol (0.1-10 mug) produced no significant effect on tremor and inconsistent results were obtained on hypothermia. 5. Neither tremor nor hypothermia were affected by 5-hydroxytryptamine (1-20 mug). 6. Oxotremorine tremor appears to be due solely to the activation of cholinergic pathways, whereas the production of hypothermia is brought about via a system involving both cholinergic and dopaminergic components. 5-Hydroxytryptamine is not involved.
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PMID:Modification of oxotremorine tremor and hypothermia by injections of drugs into the cerebral ventricles of the mouse. 101 35

Dopamine beta-hydroxylase (DBH) deficiency is a genetic disorder in which affected patients cannot synthesize norepinephrine, epinephrine, and octopamine in either the central nervous system or the peripheral autonomic neurons. Dopamine acts as a false neurotransmitter in their noradrenergic neurons. Neonates with DBH deficiency have had episodic hypothermia, hypoglycemia, and hypotension, but survivors sometimes cope relatively well until late childhood when overwhelming orthostatic hypotension profoundly limits their activities. The hypotension may be so severe that clonic seizures supervene. Most currently recognized patients are young or middle-aged adults. The diagnosis is established by the observation of severe orthostatic hypotension in a patient whose plasma norepinephrine/dopamine ratio is much less than one.
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PMID:Dopamine beta-hydroxylase deficiency. A genetic disorder of cardiovascular regulation. 167 40

1. Amphetamine-induced hypothermia in mice is facilitated by dopaminergic stimulation and 5-hydroxytryptaminergic inhibition. The present study was designed to investigate: (a) the involvement of other neuronal systems, such as the gamma-aminobutyric acid (GABA), the opioid and the cholecystokinin (CCK-8) systems; (b) the possible contribution of hydroxylated metabolites of amphetamine to the hypothermia; (c) the capacity of dopamine itself to induce hypothermia and its mechanisms, in order to clarify the resistance of amphetamine-induced hypothermia to certain neuroleptics. 2. Pretreatment with the GABA antagonists, bicuculline and picrotoxin, did not inhibit amphetamine-induced hypothermia. The GABAB agonist, baclofen (2.5 mg kg-1, i.p.) potentiated this hypothermia, whereas the GABAA agonist, muscimol, did not. gamma-Butyrolactone (GBL) (40 mg kg-1, i.p.) and the neuropeptide CCK-8 (0.04 mg kg-1, i.p.) also induced potentiation. The opioid antagonist, naloxone, was without effect. 3. Dopamine itself (3, 9, 16 and 27 micrograms, i.c.v.) induced less hypothermia than the same doses of amphetamine. Sulpiride did not block dopamine-induced hypothermia, but pimozide (4 mg kg-1, i.p.), cis(z)flupentixol (0.25 mg kg-1, i.p.) and haloperidol (5 micrograms, i.c.v.) did. The direct dopamine receptor agonist, apomorphine, did not alter the hypothermia. Neither the 5-hydroxytryptamine (5-HT) receptor blocker, cyproheptadine, nor the inhibitor of 5-HT synthesis, p-chlorophenylalanine (PCPA), modified dopamine-induced hypothermia. Fluoxetine, an inhibitor of 5-HT reuptake, had no effect, whereas quipazine (6 mg kg-1, i.p.), a 5-HT agonist, totally prevented the hypothermia. Hypothermia was unaffected by pretreatment with CCK-8. 4. These data indicate that the hypothermia induced by amphetamine involves not only dopaminergic and 5-hydroxytryptaminergic systems which are functionally antagonistic, but is also facilitated by direct or indirect GABA and CCK-8 receptor stimulation. This facilitation could result, in part, from modulation of dopaminergic neurotransmission. This may explain the apparent resistance of amphetamineinduced hypothermia to some neuroleptics, while dopamine-induced hypothermia is not resistant. The possible action of hydroxylated metabolites of amphetamine may also help to explain these differences.
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PMID:Facilitation of amphetamine-induced hypothermia in mice by GABA agonists and CCK-8. 185 28

Pancuronium is frequently used in coronary artery surgery, but its pharmacokinetics in these patients are still unknown. It is possible that dopamine, administered to prevent renal impairment induced by the surgery, might promote the elimination of pancuronium. Therefore, the pharmacokinetics of a bolus dose of pancuronium were studied in 2 groups of coronary artery surgery patients, with and without dopamine 2 micrograms/kg/min, administered during and after cardiopulmonary bypass. Dopamine in the administered dose did not influence the systemic haemodynamics. The pharmacokinetic variables in both groups did not differ from those found in an earlier study in healthy normothermic patients. Total renal clearance was not influenced by dopamine, due to post-bypass rebound hyperperfusion in the control group. Pancuronium was shown to be subject to considerable tubular reabsorption, and its elimination was found to be increased during hypothermia. Dopamine increases pancuronium elimination by an increase in glomerular filtration rate. The dopamine-induced decrease in tubular solute reabsorption did not enhance the elimination of pancuronium.
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PMID:Pharmacokinetics of pancuronium in patients undergoing coronary artery surgery with and without low dose dopamine. 229 70

We report a 42-year-old man with dopamine-beta-hydroxylase deficiency, an autonomic disorder characterized by lifelong severe orthostatic hypotension, ptosis, nasal stuffiness, hyperextensible joints, and retrograde ejaculation. There is isolated deficiency of norepinephrine in both central and peripheral neurons, which contain and release dopamine instead. Dopamine-beta-hydroxylase deficiency should be suspected also in infants presenting with delayed eye opening, hypoglycemia, hypothermia, or hypotension. It can be diagnosed definitively by assay of plasma norepinephrine and dopamine.
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PMID:Dopamine-beta-hydroxylase deficiency in humans. 230 Feb 63

The behavioral and physiological effects of repeated nicotine administration are complex; sedation and hypothermia are present early but become attenuated while locomotor activity increases. Maximal blood levels and behavioral changes occur within 10 min of s.c. injection. We examined the effects of 10 nicotine injections (0.8 mg/kg) in 14 days on the levels of brain amines following challenge with either saline or nicotine on the 15th day. Dopamine, DOPAC, HVA, 3-methoxytyramine, norepinephrine, 5-hydroxytyramine, and 5-HIAA were measured in the frontal cortex, olfactory tubercle, nucleus accumbens, caudate-putamen, substantia nigra and ventral tegmental area. Ten minutes after nicotine was given to rats that had previously received only saline the levels of dopamine and its metabolite DOPAC indicated an increase in dopamine turnover in the nucleus accumbens. Of the areas examined the accumbens was the most sensitive to nicotine, with few significant amine changes in other regions. Twenty-four hours after the last nicotine injection the levels of dopamine and its metabolites indicated a sustained decrease in dopamine turnover in the accumbens induced by repeated administration. Following repeated nicotine a nicotine challenge still induced an acute increase in dopamine turnover in the accumbens, but the response was less than in animals not previously given nicotine. The results confirm earlier studies indicating that the accumbens is a major site of nicotine action.
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PMID:Action of nicotine on accumbens dopamine and attenuation with repeated administration. 271 63

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

Dopamine, when injected into the anterior hypothalamus of the rabbit, induced a slight hyperthermia due to an upward shift of the threshold central temperature for induction of cold thermogenesis, panting and vasodilation. A slightly reduced thermosensitivity of the controller regulating vasodilation may also contribute to the hyperthermic effect of dopamine. Intrahypothalamic injections of the dopamine agonist, apomorphine, induced a similar effect to that of dopamine, with the exception that the thermosensitivity of the controller regulating vasodilation was not changed. Intraperitoneal injections of a dopamine antagonist, haloperidol, induced a marked hypothermia, due to a downward shift of the threshold central temperature for induction of cold thermogenesis, panting and vasodilation. A slightly reduced thermosensitivity of the controller regulating vasodilation was also observed. Intrahypothalamic injections of haloperidol did not induce an antagonist effect to dopamine, but rather tended to induce hyperthermia. Thermoregulatory responses, occurring after administration of dopamine or apomorphine, partially resembled those seen after administration of neurotensin or prostaglandins.
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PMID:The role of dopaminergic pathways in thermoregulation in the rabbit. 292 77

Concentrations of catecholamines in vitreous fluid and urine in guinea pigs dying of cold and the effects of freezing and autolysis on these parameters were studied. The analysis was performed by high performance liquid chromatography with electrochemical detection. Noradrenaline (NA) concentration in vitreous fluid was more than 20 times higher in the cold exposed animals than in controls (44.2 +/- 9.2 versus 2.0 +/- 1.0 ng/mL). Autolysis alone caused an increase to 33.5 +/- 7.7 ng/mL, and freezing alone to 13.4 +/- 5.3 ng/mL. The highest values were in the group with exposure, freezing, and autolysis. Adrenaline (A) concentration in the vitreous fluid increased fourfold (3.9 +/- 1.5 versus 0.7 +/- 0.5 ng/mL) in cold exposure and twofold as a result of autolysis. Dopamine (DA) concentration in vitreous fluid was elevated only in the group with exposure, freezing, and autolysis. The increase of NA concentration in urine was fivefold during the whole exposure (from 19.4 +/- 6.9 to 109 +/- 57.3 ng/mL), but A was increased by twentyfold (from 10 +/- 5.1 to 213.2 +/- 168.7 ng/mL), whereas DA concentration did not change. The increase of average excretion of NA to urine was eightfold during the first 6 h of exposure, and that of A tenfold. According to the present results, elevated concentrations of catecholamines in the vitreous fluid and urine can be used as a diagnostic aid for hypothermia death. Concerning the values of noradrenaline in the vitreous, the increase as a result of autolysis must be taken in account when interpreting the results.
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PMID:Catecholamines in the vitreous fluid and urine of guinea pigs dying of cold and the effect of postmortem freezing and autolysis. 378 3


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