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)

Administration of 10 mg/kg TRH to mice was found to reduce the sleep and hypothermia induced by 4.7 g/kg ethanol. However, TRH did not reduce the sleep of mice that were given gamma-hydroxybutyric acid (GHBA), baclophen, or aminooxyacetic acid (AOAA) in combination with 3 g/kg/ ethanol. TRH also failed to reverse the hypothermia induced by the combination of ethanol and baclophen or GHBA, and the characteristic neurological effects of TRH e.g. tremor, increased muscle tone, and increased respiratory rate were reduced. In addition, TRH-induced locomotor stimulation was prevented by pretreatment with small doses of the GABA-ergic agents, and while 30 mg/kg TRH reduced the hypothermia produced by large doses of the GABA-ergic drugs, it did not antagonize the locomotor retardation produced by baclophen or GHBA. A hypothesis that the analeptic effects of TRH may be medicated via an inhibition of GABA systems is discussed.
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PMID:Antagonism of the analeptic activity of thyrotropin-releasing hormone (TRH) by agents which enhance GABA transmission. 1 50

1. A dose-related hyperthermia is obtained in mice with TRH administered intraperitoneally. 2. This hyperthermia is reinforced by amphetamine given at doses which usually cause hypothermia. 3. p-Chloroamphetamine and L-Dopa also reinforce TRH hyperthermia. Apomorphine is not significantly active. 4. TRH hyperthermia is lowered significantly by alpha-methyl-tyrosine and haloperidol but not significantly by pimozide and chlorpromazine. TRH + Amph hyperthermia is not lowered by any of the DA antagonists tested even at doses reversing Amph hyperthermia. Direct participation of DA receptors is then doubtful. 5. All these variations of temperature have their acme a 15 min except for reserpine which, given 22 hours before, potentiates TRH + Amph hyperthermia after 30 min.
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PMID:Is a dopaminergic system involved in thyrotropin releasing hormone induced hyperthermia and in its potentiation by amphetamine? 4 68

Thyrotropin-releasing hormone (TRH), administered intraperitoneally, was found to antagonize ethanol-induced sleep and hypothermia in mice without affecting brain ethanol content. This reduction of the actions of ethanol was also apparent after oral or intracisternal administration of TRH. In addition, TRH reduced ethanol-induced sleep in rats, hamsters, gerbils and guinea pigs. Evidence that the pituitary-thyroid axis is not necessary for the effects of TRH was provided by observations that hypophysectomy did not reduce TRH antagonism of ethanol narcosis and findings that neither triiodothyronine nor thyrotropin mimicked its action. Certain analogs of TRH, which have little effect on the pituitary, were also found to antagonize ethanol-induced sleep and hypothermia. Pretreatment with the antiadrenergic drugs, alpha-methyltyrosine, phentolamine and propranolol did not antagonize the ability of TRH to reduce sleep induced by ethanol. However, after intracisternal administration of atropine methyl nitrate, TRH no longer caused a significant reduction of sleep, even though TRH antagonism of the ethanol-induced hypothermia was still apparent. In contrast, central administration of other anticholinergic drugs, such as delta-tobocurarine and hexamethonium, reduced ethanol-induced sleep and this effect was additive with TRH. Carbachol also reduced ethanol sleeping time and this effect was also blocked by atropine methyl nitrate. The antagonism of ethanol-induced sleep by dibutyryl cyclic adenosine 3', 5'-monophosphate was significantly reduced but not blocked by atropine methyl nitrate. Results provide evidence that TRH has a direct extrapituitary action on brain and that both TRH and ethanol may interact with central cholinergic systems.
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PMID:Investigations into the mechanism of reduction of ethanol sleep by thyrotropin-releasing hormone (TRH). 17 53

Cats were prepared with an array of stereotaxically implanted guide tubes, the tips of which rested just above selected structures in the brain stem. Thyrotropin-releasing hormone (TRH) was microinjected in a volume of 0.5 micronl at 347 individual sites scattered throughout the hypothalamus and mesencephalon Polypnea, hypothermia, vocalization, salivation, defecation and vasodilation were evoked by 10-20 ng of TRH injected only at loci in the mesencephalon, principally in the reticular substance. TRH failed to lower body temperature when it was infused at the same sites in the anterior hypothalamus at which norepinephrine produced its characteristic hypothermia. These results suggest that the TRH-induced hypothermia is a secondary effect of tachypnea which results from the action of the tripeptide on the mesencephalic respiratory-autonomic mechanism.
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PMID:Identification by microinjection of TRH-sensitive sites in the cat's brain stem that mediate respiratory, temperature and other autonomic changes. 40 2

Thyrotropin-releasing hormone (TRH) was found to antagonize pentobarbital-induced sleeping time and hypothermia. While 3 to 100 mg/kg of TRH reduced pentobarbital sleeping time when administered prior to the barbiturate, a dose-response relationship to TRH could not be established. However, doses of 10 to 100 mg/kg of TRH enhanced the lethality of pentobarbital when these compounds were administered simultaneously. Thyrotropin or L-triiodothyronine did not imitate and hypophysectomy did not reduce the effects of TRH, indicating that the pituitary is not essential for its antagonism of pentobarbital. Studies of TRH analogs provided further support of this view. In addition, TRH reduced the sleep and hypothermia produced by thiopental, amobarbital, secobarbital and phenobarbital, and it antagonized the hypothermia and reduced motor activity produced by chloral hydrate, reserpine, chlorpromazine and diazepam. Intracisternally administered TRH also reduced pentobarbital sleeping time and hypothermia, but melanocyte-stimulating hormone release-inhibiting factor and somatostatin administered by this route did not. While reduction of pentobarbital sleeping time by TRH could not be attributed to an affect on monoamine systems or to deamidated TRH, this action was reduced by intracisternally administered atropine, suggesting that cholinergic mechanisms may contribute to the effects of TRH. Thus, the results provide evidence that TRH acts on brain independent of an effect on the pituitary.
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PMID:Effects of thyrotropin-releasing hormone (TRH) on the actions of pentobarbital and other centrally acting drugs. 80 36

Thyrotropin releasing hormone (TRH) administered via the intracerebroventricular (icv) route in doses ranging between 0.1 and 100 mug decreased the duration of pentobarbital-induced narcosis in rabbits. Antagonism of narcosis occurred whether TRH was administered before or after the barbiturate. TRH doses above 10 mug produced, in addition, behavioral excitation and hyperthermia. The antagonism of phenobarbital-induced narcosis was not as profound; animals were aroused only for a short period of time, after which the narcotized state returned. However, TRH exerted a prolonged antagonism or reversal of the phenobarbital-induced hypothermia. The central nervous system depression and analgesia produced by morphine were unaffected by TRH, but hypothermia and respiratory depression were reversed. TRH may represent an arousal factor in mammalian brain.
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PMID:Influence of thyrotropin releasing hormone (TRH) on drug-induced narcosis and hypothermia in rabbits. 82 48

The effect of TRH on pentobarbital narcosis in 21 rhesus monkeys was examined. Vital signs monitored included respiration rate, heart rate, temperature, sleeping time,and time of reappearance of certain reflexes. Blood samples were obtained for pentobarbital assay. Two dose schedules for TRH administration were used. One group of 6 animals received a single dose of 20 mg/kg 30 min after barbiturate administration, while the other group were received 3 injections of 20 mg/kg spaced at 30, 40 and 50 min after injection of pentobarbital. Both groups were sex balanced. TRH administration resulted in dramatically increased respiration and heart rates and arrested the progress of barbiturate induced hypothermia. The extended dose schedule prolonged increased respiration rate and a differential effect of TRH on pentobarbital induced hypothermia across sexes was observed. All animals regained reflexes sooner and sleeping time was reduced by 22%. No differences in pentobarbital blood levels with TRH were observed. These results extend earlier work in rodents to primates and suggest a possible use of TRH in cases of acute barbiturate intoxication.
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PMID:Thyrotropin releasing hormone: antagonism of pentobarbital narcosis in the monkey. 82 52

The pathophysiological changes associated with hypothermia were investigated in the rat stomach under anesthetized conditions. The animal was placed in a styrene foam box and the core body temperature was kept between 24 and 36 degrees C using a heat lamp and refrigerant pack. Lowering of body temperature (less than 30 degrees C) produced acid hypersecretion and induced hemorrhagic lesions in the gastric mucosa; these responses reached the maximum at 28 degrees C, and a significant relationship was found between acid output and lesion score. Hypothermia (28 degrees C) also caused a marked increase of gastric contractile activity and mucosal blood flow (MBF), but the ratio of acid output to MBF became greater when compared to that obtained under normothermic conditions. These changes induced by hypothermia (28 degrees C) were completely blocked by vagotomy and were significantly inhibited by atropine, hexamethonium, clonidine, or TRH antiserum. However, lowering body temperature did not significantly affect acid secretory, motility, and ulcerogenic responses induced by carbachol in the vagotomized rat, excluding local mechanisms (suppression of the inhibitory nerves) in the hypothermia-induced changes. We conclude that hypothermia alone stimulates vagally dependent acid secretion and motility, resulting in damage in the gastric mucosa. These changes may be centrally mediated by TRH, which is released in association with the thermogenic response to hypothermia.
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PMID:Vagally mediated acid hypersecretion and lesion formation in anesthetized rat under hypothermic conditions. 167 16

The behavioral effects of the TRH analogue RX77368, dimethyl proline-TRH (3, 10 and 30 mg/kg IP), in 5-, 10- and 20-day-old rat pups were investigated. The peptide induced shaking behavior and increased locomotion as early as 5 days after birth. At 20 days RX77368 also produced rearing, stereotyped mounting and grooming (mainly licking and chewing of the forepaws). Additionally, RX77368 produced hypothermia and antinociception in the infant rats. These responses, which were generally, although not always, comparable with those found in adults, agree with biochemical studies showing high levels of TRH receptors in the brain and spinal cord in the first three weeks following birth.
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PMID:Behavioral profile of the TRH analogue RX77368 in developing rats. 212 22

The central action, particularly potential antidepressant activity of WEB 1881, a new nootropic drug related to piracetam, was investigated in rats and mice. WEB 1881 antagonizes the reserpine- and apomorphine-induced hypothermia, potentiates the behavioral effect of DOPA and dihydroxyphenylserine, as well as the TRH-induced hyperthermia. Piracetam was only effective in the reserpine and DOPA tests. WEB 1881 is inactive in immobility test of Porsolt et al. It enhances the hind limb flexor reflex of the spinal rat, this effect being antagonized by prazosin and cyproheptadine. It exerts no effect on head twitches induced by L-5-hydroxytryptophan. The studied compound increases the noradrenaline and dopamine and turnover in the forebrain and brain stem. WEB 1881 given repeatedly potentiates the clonidine-induced aggressiveness and has no effect on the locomotor hyperactivity induced by D-amphetamine. The results indicate that in a number of tests WEB 1881 acts like other antidepressant drugs (but in others not), moreover, they suggest that this action is--at least partly--mediated by the central noradrenaline system.
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PMID:Antidepressant activities of WEB 1881, a new nootropic agent. 256 89


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