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 intraventricular administration of thyrotropin-releasing hormone (TRH) to conscious rabbits produces a dose-related increase in body temperature, a compulsive scratching syndrome, and behavioral excitation. These effects are not antagonized by most adrenergic or serotonergic blockers, amine depletors, or most depressants. Given to rabbits pretreated with anesthetic doses of barbiturates or high doses of other sedatives or neuroleptics, TRH exerts an analeptic effect. The duration of pentobarbital anesthesia is markedly shortened. Of all the depressants tested, only morphine was resistant to the analeptic effect of TRH, although the morphine-induced hypothermia was reversed.
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PMID:Thyrotropin-releasing hormone (TRH)-induced hyperthermia and behavioral excitation in rabbits. 81 76

Acid secretory and mucosal ulcerogenic responses to hypothermia (36-24 degrees C) were examined in anesthetized rats, and the role of thyrotropin-releasing hormone (TRH) in these responses was investigated. Lowering of body temperature (less than 32 degrees C) induced acid hypersecretion and damage in the gastric mucosa. These responses reached a maximum at a body temperature of 28 degrees C and were completely abolished by bilateral cervical vagotomy and significantly inhibited by intracerebroventricular (i.c.v.) administration of TRH antiserum (10 microliters/rat). TRH (10 micrograms/rat) given i.c.v. to the normothermia rat, caused an increase of acid secretion with a pattern similar to those observed during hypothermia. The blood levels of thyroid-stimulating hormone rose significantly during exposure of cold, and this response preceded the onset of acid hypersecretion and lesion formation. Thus, lowering of body temperature induces vagal-dependent gastric acid secretion, probably mediated by TRH released in response to cold exposure, and may be an important element in the etiology of stress ulceration.
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PMID:Role of thyrotropin-releasing hormone in acid secretory response induced by lowering of body temperature in the rat. 190 61

A series of thyrotropin-releasing hormone (TRH) analogues in which the pyroglutamic acid residue was replaced by (S)-4,5-dihydroorotic acid (Dio-OH) and the related derivatives were prepared. Their central nervous system actions based on spontaneous locomotor activity, antagonistic effect on reserpine-induced hypothermia, and antagonistic effect on pentobarbital anesthesia were evaluated and the structure-activity relationships are discussed. Of these, (1-methyl-(S)-4,5-dihydroorotyl)-L-histidyl-L-prolinamide (14b) showed the most potent activities, which were 30-90 times greater than those of TRH. Moreover, the thyrotropin-releasing activity of 14b was about 50 times weaker than that of TRH, and compound 14b (TA-0910) was selected as a potent candidate.
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PMID:Synthesis and central nervous system actions of thyrotropin-releasing hormone analogues containing a dihydroorotic acid moiety. 211 88

Effects of orally administered TA-0910, a new thyrotropin-releasing hormone (TRH) analog, on the central nervous system (CNS) were investigated and compared with those of TRH. TA-0910 shortened the duration of pentobarbital-induced sleep and antagonized reserpine-induced hypothermia at 0.3 mg/kg or more in mice. TA-0910 enhanced the spontaneous motor activity at the higher dose of 30 mg/kg in mice. The drug also activated acute spontaneous EEGs in rabbits at 1 mg/kg. TRH produced these effects at about 100 times higher doses than TA-0910. In antagonizing pentobarbital-induced sleep, the dose ratios of i.v. versus p.o. of TA-0910 and TRH were about 1/10 and 1/100, respectively. The duration of the antagonistic action of TA-0910 on pentobarbital-induced sleep in mice was about 8 times longer than that of TRH when administered orally as well as intravenously. These potent and long-acting TA-0910 effects on the CNS are discussed in connection with its biotransformation.
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PMID:Pharmacological study of TA-0910, a new thyrotropin-releasing hormone (TRH) analog, (I): Effects on the central nervous system by oral administration. 212 Apr 94

It has been suggested that a nonapeptide called V-9-M (Val-Pro-Val-Glu-Ala-Val-Asp-Pro-Met) is produced by the processing of procholecystokinin. However, its physiological and pharmacological activities are not known. In the present study, synthetic V-9-M amide was injected into the lateral ventricle of the rat and its effects on general activities were observed. V-9-M caused a marked sedation; it suppressed spontaneous activity and hypermotility induced by thyrotropin-releasing hormone, methamphetamine, and apomorphine. Hypomotility induced by small doses of apomorphine was also decreased further. V-9-M caused hypothermia and prolonged the duration of pentobarbital-induced sleep, and it decreased locomotion in an open-field situation. However, V-9-M did not affect appetite in fasted rats.
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PMID:Neuropharmacological properties of V-9-M, a putative neuropeptide derived from procholecystokinin, in the rat. 250 Oct 13

Measurements of basal body temperature obtained from first-morning voided urine were followed longitudinally in 23 individuals with anorexia nervosa. In each of 10 hypothermic individuals, we found that basal body temperature was significantly correlated with weight gain, whereas in most normothermic individuals, no relationship was found. This suggests that measurement of basal body temperature may provide a convenient means of assessing clinical improvement and nutritional rehabilitation in some patients with anorexia nervosa. Differences in neuroendocrine measures and weight gain were also studied. Thyroid functions did not differ significantly between groups, and no differences were found in dexamethasone suppression or in the thyrotropin-releasing hormone (TRH) stimulation test. Hypothermic individuals, however, were significantly younger and significantly more likely to gain weight in response to treatment.
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PMID:Urinary basal body temperature in anorexia nervosa. 274 44

The effects of microinjections of thyrotropin-releasing hormone (TRH), neurotensin and ICI 174864 into the nucleus accumbens, nucleus caudatus, septum and mesencephalic periaqueductal grey were studied on ethanol-induced narcosis in the rat. Levels of narcosis were assessed by alterations in ethanol-induced hypothermia and sleep time. Ethanol produces a 2 degree C fall in body temperature over the first hour which then recovered over the next 2 h. Sedation was produced to the extent that the righting reflex was lost for between 80 and 90 min. In the nucleus caudatus all 3 peptides were ineffective at altering narcosis. In the periaqueductal grey, septum and accumbens, TRH (5 micrograms) and ICI 174864 (1 microgram) microinjections significantly reduced the sleep time by between 50 and 70%. ICI 174864 was approximately 10 times more potent that TRH at reducing the sleep time. In addition, both these peptides significantly accelerated the recovery from the ethanol-induced hypothermia in the periaqueductal grey, septum and accumbens. ICI 174864 prevented the ethanol-induced fall in body temperature. Neurotensin (5 micrograms) significantly increased the sleep time by up to 50% and potentiated the ethanol-induced hypothermia. These results suggest that the administration of TRH or the blockade of delta-opioid receptors, resulting in an inhibition of endogenous enkephalin transmission, may significantly inhibit ethanol narcosis in the rat. Opposing this, the application of neurotensin appears to potentiate ethanol narcosis. These results also indicate that endogenous enkephalin release plays an important role in ethanol narcosis.
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PMID:The effect of neurotensin, TRH and the delta-opioid receptor antagonist ICI 174864 on alcohol-induced narcosis in rats. 282 97

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

Administration of capsaicin (CAP) and its related pungent, nonanoyl vanillylamide (NVA) produced significant dose-dependent hypothermic response in mice at an ambient temperature of 24 degrees C. CAP was approximately equieffective to NVA in producing hypothermia. After large doses, desensitization occurred to the hypothermic effects of both CAP and NVA. The hypothermia produced by CAP and NVA was prevented by a small dose of thyrotropin-releasing hormone (TRH) (0.25 nmol/animal) which by itself had little effect on body temperature. Histidyl-proline diketopiperazine, a metabolite of TRH, was without effect on the hypothermic response of CAP and NVA. The result suggests that a TRH neuronal system in the brain may explain a part of the mechanism of CAP- and NVA-induced hypothermia in mice.
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PMID:Studies on the hypothermic response of capsaicin and its analogue in mice. 308 4

The effects of thyrotropin-releasing hormone (TRH) and its putative metabolite, cyclo-histidine-proline (cHP), on the homeothermic development of neonatal rats were studied. The daily intrathecal administration of 10(-11)-10(-9) moles of TRH during the second week of age produced a significant rise in body temperature by 3 weeks of age and was followed by a transient period of hypothermia. This effect, which could not be produced by an intraperitoneal injection of 10(-7) moles of TRH, was abolished by the simultaneous administration of 6-hydroxydopamine (6OHD). In contrast, intrathecally administered cHP decreased thermogenesis. During TRH treatment, brain norepinephrine (NE) and dopamine (DA) release was accelerated 2- to 4-fold. Two weeks after either TRH or cHP treatment, brain NE and DA were significantly reduced; adrenal NE in cHP-treated rats increased. The weight of the interscapular brown adipose tissue (BAT) was decreased by both cHP and 6OHD. At 3 weeks of age, [3H]guanosine diphosphate binding capacity in BAT mitochondria was reduced by 60% in TRH-treated rats and was associated with reduced mitochondrial levels of alpha-glycerophosphate dehydrogenase and liver cytochrome C reductase. These results indicate that TRH stimulates central NE release thereby enhancing thermogenesis, cHP decreases heat production, and TRH-induced hyperthermia is associated with changes in mitochondrial exothermic processes. The central TRH-cHP system may modulate the maturation of homeothermic mechanism in neonatal rats.
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PMID:Effects of thyrotropin-releasing hormone and cyclo-histidine-proline on the homeothermic development of neonatal rats. 309 34


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