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)

Lisuride hydrogen maleate induced stereotyped behaviour in normal as well as in reserpinized mice. It antagonized the motor depression and hypothermia induced by reserpine. On i.p. administration the compound was about as effective as apomorphine and D-amphetamine. As with apomorphine and in contrast to D-amphetamine the effects of lisuride hydrogen maleate in reserpinized mice were not impaired by additional treatment with alpha-methyl-p-tyrosine methylester. In untreated mice, the substance was very potent in lowering body temperature with significant hypothermia measured after dosages as low as 0.10 mg/kg i.p. Occurrence of stereotyped behaviour and hypothermia could be prevented by the dopaminergic antagonist haloperidol. From these data it is concluded that lisuride hydrogen maleate in addition to its interaction with serotoninergic systems is a potent dopaminergic agonist with a probably direct action on dopaminergic receptors. Further arguments in support of such an action of lisuride hydrogen maleate are, in addition to biochemical data, its serum prolactin lowering effect in rats, its strong emetic action in dogs and its effects on rat behaviour.
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PMID:Direct dopaminergic action of lisuride hydrogen maleate, an ergot derivative, in mice. 94 66

Craniocerebral hypothermia was used in the treatment of 43 women aged 48 to 55, suffering from the climacteric syndrome of varying severity. The treatment efficacy was confirmed by EEG data and changes in blood levels of ACTH, LH, prolactin, and hydrocortisone.
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PMID:[Effects of craniocerebral hypothermia on the course of climacteric syndrome]. 132 Mar 45

Administration of 8-hydroxy-2(di-n-propylamino)tetralin (8-OHDPAT) to rats produced dose-dependent decreases in food intake and hypothermia, increases in plasma prolactin and corticosterone, and a decrease in plasma growth hormone. 8-OHDPAT administration also induced the serotonin behavioral syndrome at all doses. Pretreatment with metergoline did not affect the 8-OHDPAT-induced behavioral syndrome or decrease in food intake but attenuated the prolactin increase and, furthermore, potentiated 8-OHDPAT-induced hypothermia. Pretreatment with ritanserin or naloxone did not modify 8-OHDPAT-induced changes in food intake, temperature or prolactin. Similarly, pretreatment with phenoxybenzamine, propranolol, clonidine, haloperidol and methiothepin also did not attenuate 8-OHDPAT-induced decreases in food intake. Administration of pindolol alone produced hyperthermia, decreased food intake and enhanced prolactin secretion. Pindolol thus appears to act as a partial 5-HT agonist in addition to being an antagonist at central 5-HT receptors.
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PMID:Food intake, neuroendocrine and temperature effects of 8-OHDPAT in the rat. 296 88

Thyroid hormone serum concentrations, the thyrotropin (TSH) and prolactin (PRL) response to thyrotropin-releasing hormone (TRH) were evaluated in patients undergoing cardiopulmonary bypass (CPB) conducted in hypothermia. During CPB a marked decrease of thyroxine (T4) and triiodothyronine (T3) concentration with a concomitant increase of reverse T3 (rT3) were observed similarly to other clinical states associated with the 'low T3 syndrome'. Furthermore, in the present study elevated FT4 and FT3 concentrations were observed. In a group of patients, TRH administered during CPB at 26 degrees C elicited a markedly blunted TSH response. In these patients, PRL concentration was elevated but did not significantly increase after TRH. The increased concentrations of FT4 and FT3 were probably due to the large doses of heparin administered to these patients. Thus, the blunted response of TSH to TRH might be the consequence of the elevation of FT4 and FT3 in serum, however, other factors might play a role since also the PRL response to TRH was blocked.
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PMID:Cardiopulmonary bypass: a low T4 and T3 syndrome with blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH). 308 19

In order to investigate neuroendocrinological mechanisms of hypothermia, we determined the changes in plasma concentrations of corticosterone (CS), prolactin (PRL), and thyrotropin (TSH), and their correlations with alterations in hypothalamic dopamine (DA) and thyrotropin releasing hormone (TRH), in rats restrained and immersed in a water bath at various temperatures. A graded decrease of body temperature induced a progressive increase in the plasma level of CS, whereas that of PRL showed a drastic decrease. The plasma level of TSH also showed an increase during mild hypothermia (about 35 degrees C), but this increase was not evident during profound hypothermia (below 24 degrees C). The changes in these hormones were readily reversed by rewarming animals. Although DA content in the hypothalamus was not affected, its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), showed an increase following the decrease of body temperature. Pretreatment of the animals with sulpiride, a D2-antagonist, prevented the hypothermia-induced inhibition of PRL release. Hypothalamic TRH was significantly decreased during mild hypothermia, and it returned to control levels after rewarming. These results suggest that the decrease in plasma PRL induced by hypothermia may be associated with the activation of hypothalamic DA neurons, whereas the increase in plasma TSH during mild hypothermia seems to be caused by the increased release of TRH in the hypothalamus.
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PMID:Hypothalamic control of pituitary and adrenal hormones during hypothermia. 310 46

The effects of analgesic, thermoregulatory and endocrine functions of administering morphine sulphate (0.3 mg) into the lateral cerebral ventricle via an Ommaya catheter were assessed in eight patients with cancer pain. Satisfactory control of intractable pain was obtained in these patients, without any change in other sensory modalities. The delay in the onset of pain relief and the duration of analgesia ranged, respectively, from 20 to 40 min and from 12 to 16 h after drug injection. In addition, intraventricular administration of morphine caused a reduction in rectal temperature in these patients at an ambient temperature of 24 degrees C. The hypothermia in response to the injection of morphine was due to cutaneous vasodilation and sweating. There was no change in metabolism or in respiratory evaporative heat loss after morphine injection. Further, 10 to 20 min after intraventricular administration of morphine, the blood levels of prolactin, growth hormone and glucose were elevated in these patients. The changes in temperature and endocrine levels lasted for 1-3 h. In addition to the pain relief, these side-effects of morphine treatment were short-lasting and disappeared as the morphine treatment continued. The results indicate that activation of opiate receptors in the brain produced pain relief, hypothermia (due to cutaneous vasodilation and sweating), and increased blood levels of prolactin, growth hormone and glucose in patients with cancer pain.
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PMID:Intraventricular morphine produces pain relief, hypothermia, hyperglycaemia and increased prolactin and growth hormone levels in patients with cancer pain. 343 Jan 86

Cholinesterase inhibitors induce changes in plasma hormones in the rat. Since these compounds induce hypothermia the question has been raised as to whether the endocrine responses are secondary to the fall in core temperature. The time course of the changes in temperature and plasma levels of corticosterone, growth hormone and prolactin have been examined following injection of diisopropylphosphofluoridate (DFP), soman or physostigmine. All three cholinesterase inhibitors caused an initial rise in corticosterone; DFP decreased growth hormone; physostigmine reduced prolactin. The time course of the hypothermia after DFP and soman did not correlate with that of the rise in corticosterone. The data do not suggest that the hormone changes are secondary to the temperature change.
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PMID:Relationship between the temperature and endocrine changes induced by cholinesterase inhibitors. 358 58

It has been demonstrated that nutritional iron-deficiency induced in rats results in the reduction of DA D2 receptor binding sites, leading to down-regulation of dopaminergic activity similar to that observed in neuroleptic-treated animals. The following observations are common to both conditions: (a) Decreased behavioural response to pre- and post-synaptically DA and serotonin acting drugs, amphetamine, apomorphine and 5-methoxy-N,N-dimethyltryptamine. (b) Inhibition of amphetamine or apomorphine induced hypothermia in rats kept at an ambient temperature of 4 degrees C. (c) Increased sleeping time to phenobarbitone which cannot be attributed to the rate of drug metabolism (5,38). (d) Upregulation of prolactin binding sites in the liver as a result of increased serum prolactin. Additionally, nutritional iron-deficiency lowers brain iron and interferes with protein synthesis in this organ, which could explain the reduction of DA D2 receptor number and function. Given the fact that the highest brain concentrations of iron are found in dopaminergic structures (see 42 for review), and the essential role of intact dopaminergic systems to attentional and learning processes (15b,30), the resultant behavioural changes due to the reduction of dopaminergic activity in iron-deficient animals may go some way to explain the adverse effects on cognition, behavioural patterns, learning and attention, event-related potentials (ERPs) and EEG changes reported in iron-deficient children (19-28,30).
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PMID:Brain iron and dopamine receptor function. 613 53

The effects of direct administration of TRH, TSH, LHRH, LH, ACTH, GH, FSH and prolactin into cerebral ventricle system on metabolic, respiratory, cardiovascular and behavioral responses were assessed in unanesthetized rats, Intraventricular administration of TRH, TSH, LHRH or LH caused hypothermia, decreased metabolism and/or cutaneous vasodilation at room temperature (22 degrees C). Intraventricular administration of FSH, ACTH or prolactin caused hyperthermia, increased metabolism and/or cutaneous vasoconstriction. Intraventricular administration of GH caused an insignificant change in thermoregulatory responses. There was no change in respiratory evaporative heat loss in response to either of the drugs tested. In addition, intraventricular administration of TRH, LHRH or LH caused tachycardia, hypertension and a reduction in the epinephrine-induced reflex bradycardia. In contrast, intraventricular administration of prolactin caused bradycardia, hypotension and an enhancement in the epinephrine-induced reflex bradycardia in conscious rats. There was no change in cardiovascular function in response to intraventricular administration of TSH, FSH, ACTH or GH. Furthermore, following intraventricular administration of TRH, but not TSH, LHRH, LH, FSH, GH, ACTH or prolactin three main categories of behavior were provoked: activity of normal type--forward locomotion stimulation, head and body rearing; stereotype activity--increased grooming and head swaying; and abnormal type behavior--tail elevation and piloerection in rats. The data indicate that most of the anterior pituitary hormones and their releasing hormones act through a central mechanism to influence physiological and/or behavioral functions.
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PMID:Effects of anterior pituitary hormones and their releasing hormones on physiological and behavioral functions in rats. 635 Jul 20

2-Bromolisuride (2-Br-LIS), a derivative of the ergot dopamine (DA) agonist lisuride, was investigated in rodents in comparison with the DA antagonist haloperidol with regard to its influence on DA related behaviour, cerebral DA metabolism and prolactin (PRL) secretion. 2-Br-LIS produced catalepsy in mice (ED50 3.3 mg/kg i.p.), antagonized apomorphine-induced stereotypies in mice (ED50 0.4 mg/kg i.p.), antagonized DA agonist-induced stereotypies in rats (0.1-1.56 mg/kg i.p.), inhibited locomotor activity in rats (0.025-6.25 mg/kg i.p.), antagonized the hyperactivity produced by various DA agonists in rats (0.025-6.25 mg/kg i.p.) and inhibited the apomorphine-induced hypothermia in mice (0.05-0.78 mg/kg i.p.). 2-Br-LIS (0.03-10 mg/kg i.p.) stimulated DA biosynthesis and DOPAC formation in the striatum and DA rich limbic system of rats, but had no effect on serotonin turnover. In striatum and limbic forebrain of gamma-butyrolactone-pretreated rats 2-Br-LIS reversed the apomorphine-induced inhibition of DOPA accumulation. 2-Br-LIS (0.03 - 3 mg/kg) enhanced PRL secretion in intact male rats. These findings indicate DA antagonistic properties of 2-Br-LIS presumably due to blockade of central pre- and postsynaptic DA receptors being of approximately the same order of potency as haloperidol. 2-Br-LIS is the first ergot compound with definite antidopaminergic properties suggesting its potential usefulness as a neuroleptic.
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PMID:Central antidopaminergic properties of 2-bromolisuride, an analogue of the ergot dopamine agonist lisuride. 660 92


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