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)

In this study we have examined the interactions of bombesin (1 microgram ICV), neurotensin (1 microgram ICV), TRH (10 micrograms ICV), somatostatin (10 micrograms ICV), PGE2 (10 micrograms ICV) and naloxone (10 mg/kg SC) on thermoregulation in the rat at room temperature (20 +/- 1 degree C). Given alone, bombesin, neurotensin, somatostatin and naloxone all produced hypothermia (bombesin greater than neurotensin greater than somatostatin congruent to naloxone). PGE2 was hyperthermic, and TRH had no effect. Bombesin and PGE2 neutralized one another's effects. Neurotensin had no effect on PGE2-induced hyperthermia. Naloxone enhanced the hypothermic effect of bombesin and somatostatin enhanced the rate of onset of hypothermia after bombesin. TRH had no effect on bombesin-induced hypothermia. TRH, somatostatin and naloxone had no effect on neurotensin-induced hypothermia. TRH antagonized the hypothermia due to naloxone and somatostatin.
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PMID:Neuropeptides and thermoregulation: the interactions of bombesin, neurotensin, TRH, somatostatin, naloxone and prostaglandins. 612 11

An intracisternal injection of somatostatin-28 produced hyperthermia in rats at cold, thermoneutral, warm ambient temperatures. The hyperthermic response to somatostatin-28 was not prevented by pretreatment of rats with the following agents: alpha-methylparatyrosine, phenoxybenzamine, propranolol, sulpiride, atropine, methysergide or naloxone. Somatostatin-28 prevented hypothermia induced by bombesin and gamma-MSH when it was administered simultaneously, but it left the hyperthermic response to TRH intact. The results indicate that somatostatin-28 produces hyperthermia by elevating a "set point" or regulated level of temperature. Under the conditions tested, the hyperthermic response to somatostatin-28 does not appear to be dependent on muscarinic cholinergic, serotonergic, alpha- or beta-adrenergic, dopaminergic or endogenous opiate system.
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PMID:Hyperthermic action of somatostatin-28. 613 57

Well established as supposed antidepressant drugs, desipramine (1.25-5 mg/kg), nisoxetine (0.625-2.5 mg/kg) and clomipramine (1.25-5 mg/kg) but not fluoxetine (2.5-40 mg/kg) or citalopram (2.5-40 mg/kg) dose-dependently potentiated TRH (40 mg/kg)-induced hyperthermia in mice. Alpha-adrenergic blocking agents, phenoxybenzamine (20 mg/kg) and prazosin (5 mg/kg), which when given alone lowered body temperature, did not prevent the thermogenic effect of TRH but completely abolished the potentiating effect of clomipramine and almost completely antagonized the same effect of desipramine. The potentiating effect of desipramine on TRH-induced hyperthermia was also attenuated by 4 mg/kg l-propranolol but not by the same dose of d-propranolol. l-Propranolol (4 mg/kg) did not affect the potentiating effect of clomipramine. Cyproheptadine (5 mg/kg), an antagonist of 5-hydroxytryptamine receptors (which, like the alpha-adrenoceptor antagonist, produced hypothermia in normal mice) did not prevent the effects of clomipramine or desipramine. We conclude that a noradrenergic rather than a 5-hydroxytryptaminergic mechanism is involved in the potentiating effect of antidepressant drugs on TRH-induced hyperthermia. Hence, screening tests for antidepressants, which are based on the potentiation of the TRH-induced hyperthermia will always result in false negatives for antidepressants, such as citalopram, which are highly selective inhibitors of the uptake of 5-hydroxytryptamine.
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PMID:The effect of highly selective inhibitors of the uptake of noradrenaline or 5-hydroxytryptamine on TRH-induced hyperthermia in mice. 613 92

The interactions of thyrotropin releasing hormone, its metabolites and synthetic analogues with acute and chronic effects of endogenous and exogenous opiates have been described. The endogenous and exogenous opiates are represented by beta-endorphin and morphine, respectively. The pharmacological effects of opiates include analgesia, temperature effects, respiratory depression, catalepsy, locomotor activity, opiate receptor binding, tolerance, and physical dependence. Thyrotropin releasing hormone and related compounds appear to (a) antagonize hypothermia, respiratory depression, locomotor depression and catalepsy but not the analgesia induced by opiates, (b) inhibit the development of tolerance to the analgesic effect but not to the hypothermic effect of opiates, (c) inhibit the development of physical dependence on opiates as evidenced by the inhibition of development of certain withdrawal symptoms, and (d) suppress the abstinence syndrome in opiate dependent rodents. Thyrotropin releasing hormone does not interact with the opiate receptors in the brain. Potential therapeutic applications of thyrotropin releasing hormone and its synthetic analogues in counteracting some of the undesirable effects of opiates are discussed.
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PMID:Interactions of thyrotropin releasing hormone, its metabolites and analogues with endogenous and exogenous opiates. 614 Nov 21

The effect of intracerebral injection of TRH and several biologically stable TRH analogues in the pentobarbitone anaesthetized rat was examined. Bilateral injection of TRH (5.0 micrograms total dose) and the analogues RX 77368 (0.01-1.0 microgram), CG 3509 (0.1-1.0 microgram), DN-1417 (1.0 microgram) and MK-771 (1.0 microgram) into the nucleus accumbens reduced the pentobarbitone-induced sleeping time. The TRH metabolite DKP (5 micrograms) had no effect on the sleeping time following intra-accumbens injection. Intra-septal injection of TRH (1.0-5.0 micrograms), RX 77368 (0.1-1.0 microgram) and CG 3509 (0.1-1.0 microgram) also reversed the pentobarbitone-induced sleeping time. In contrast, TRH (5 micrograms) injected into the striatum had no effect on the pentobarbitone-induced sleeping time, and CG 3509 (0.1 microgram) and RX 77368 (0.1 microgram) had weaker effects following intrastriatal injection compared to injection of these analogues into the nucleus accumbens and septum. Measurements of core temperature and respiration rate in rats following intra-accumbens or septal injection of TRH, CG 3509 and RX 77368 showed these peptides to reverse pentobarbitone-induced hypothermia and stimulate respiration rate. However, while intrastriatal injections of CG 3509 and RX 77368 caused an increase in respiration rate they had no effect on core temperature. These results suggest a close association between peptide-induced respiratory stimulation and reversal of pentobarbitone-induced anaesthesia. Since intra-accumbens and septal injection of dopamine (20-100 micrograms) failed to reverse anaesthesia, it is unlikely that the peptide-induced responses are mediated via dopamine release.
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PMID:Analeptic effects of centrally injected TRH and analogues of TRH in the pentobarbitone-anaesthetized rat. 614 13

Zimelidine and norzimelidine were tested for their ability to counteract reserpine (2.5 mg kg-1)- or apomorphine (1-16 mg kg-1)-induced hypothermia and to potentiate TRH (40 mg kg-1)-induced hyperthermia in mice. Norzimelidine produced positive results in all three tests, behaving like a weak NA uptake inhibitor. Zimelidine was practically inactive. We conclude that the weak inhibitory effect of norzimelidine on the uptake of NA (in-vitro experiments) may be of importance for its pharmacological action and for the clinical action of zimelidine.
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PMID:Norzimelidine, a metabolite of a highly selective 5-hydroxytryptamine uptake inhibitor, can inhibit the uptake of noradrenaline in-vivo. 615 86

Cholecystokinin-octapeptide (CCK-8) was shown to cause hypothermia after intracerebroventricular administration in the rat, and the hypothermic effect of CCK-8 was antagonized by simultaneous injection of TRH.
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PMID:Cholecystokinin-induced hypothermia in the rat. 625 73

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

Thyrotropin-releasing hormone (TRH), a hypothalamic polypeptide, will antagonize some of pentobarbital's major effects (sleep time and hypothermia) in rodents when administered in low doses (1-10 mg/kg). At higher doses (30 and 100 mg/kg), TRH has been shown to increase the lethality of high doses of pentobarbital in mice. The present experiments demonstrated that 10 mg/kg of TRH will potentiate the conditioned flavor aversion normally induced in rats by 20 mg/kg of pentobarbital, suggesting that the TRH-pentobarbital combination may have sublethal toxic effects even at low doses of both substances. Furthermore, this result suggests that the mechanism whereby pentobarbital produces a flavor aversion is independent of the drug's hypothermic and sleep-inducing effects.
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PMID:Thyrotropin-releasing hormone (TRH) potentiates pentobarbital-based flavor aversion learning. 641 19

Intracerebroventricular (ICV) administration of kyotorphin (L-Tyr-L-Arg) and cyclo (N-methyl-L-Tyr-L-Arg), its analog, produced significant dose-dependent hypothermic responses in mice at an ambient temperature of 24 degrees C. The hypothermic action of kyotorphin was much greater than that of Met-enkephalin (Met-ENK) but less than that of cyclo NMTA. This action was slightly but not significantly reversed by intraperitoneally administered naloxone (8 mg/kg), an opioid receptor antagonist. Met-ENK utilized as a control peptide in this study also produced a dose-dependent hypothermia which was slightly antagonized by naloxone (8 mg/kg, IP). Thyrotropin releasing hormone (TRH) injected ICV produced hyperthermia dose-dependently. The hypothermia induced by kyotorphin, its cyclic analog and Met-ENK was prevented by a small dose of TRH (0.18 microgram = 0.5 nmol/animal) which by itself had little effect on body temperature. A TRH neuronal system in the brain may explain the mechanism of kyotorphin-induced hypothermia. However, there was little evidence of involvement of opioid receptors. The present study demonstrates a potent action of kyotorphin and its analog on thermoregulation.
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PMID:Actions of intracerebroventricular administration of kyotorphin and an analog on thermoregulation in the mouse. 642 2


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