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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of narcotic analgesics on the brain 5-hydroxytryptamine (5-Ht) and 5-hydroxyindoleacetic acid (5-HIAA) levels of rats and mice were investigated in relation to our preceding data on the effect of humoral modulatorents. The results suggest that morphine accelerates the release of brain 5-HT both in rats and mice, and that neither methadone nor pethidine alters the brain 5-HT and 5-HIAA levels in rats. The morphine-induced increase in brain 5-HT turnover is likely to be involved in the morphine-induced decrease in locomotor activity and hypothermia in rats. The activity-decreasing effects of methadone or pethidine, on the other hand, are mediated by mechanisms different from those which mediate the effects of morphine. In contrast, an increase in brain 5-HT turnover in mice apparently does not play an important role on activity-increasing effects of morphine but rather participates in other pharmacological effects of morphine.
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PMID:Effects of narcotic analgesics on serotonin metabolism in brain of rats and mice. 1 94

Cessation of chronic ethanol administration, and elimination of ethanol from the body, results in a withdrawal syndrome in mice characterized by behavioural symptoms and hypothermia. During withdrawal, the accumulation rate of [14C] 5-hydroxytryptamine (5-HT) from [14C]tryptophan, was significantly lower in the brainstem of the ethanol-withdrawn animals than in controls. A similar pattern was seen in forebrain. When the rate of 5-HT accumulation was determined using pargyline, no differences occurred between control and ethanol-treated animals. The endogenous concentrations of tryptophan in plasma, and tryptophan, 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) in brain were the same in ethanol-treated and control animals. It is suggested that the changes in accumulation of 14C-5-HT and 14C-5-HIAA in ethanol-withdrawn animals reflected alterations in electrical activity of serotoninergic neurons during withdrawal.
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PMID:Neurochemical correlates of ethanol withdrawal: alterations in serotoninergic function. 1 95

A single injection of phenelzine 100 mg kg-1 given 18 h before, decreased the analgesia and hypothermia induced by morphine, but potentiated the analgesic and hypothermic effects of pethidine, when the analgesics were administered either intraperitoneally, or intracerebroventricularly. The modification of pethidine analgesia and hypothermia, but not morphine analgesia, was antagonized by methysergide (10 mg lg-1, s.c.). The LD50 of pethidine, but not that of morphine, was 30-40% lower in mice treated with phenelzine tranylcypromine or iproniazid 6 h before the test. The increased lethality of a single dose of pethidine induced by phenelzine was also prevented by methysergide. Pretreatment of mice with 100 mg kg-1 phenelzine was followed by a significant rise in both brain tryptophan and 5-hydroxytryptamine (5-HT) concentrations which lasted for 24 h. Therefore, the changes in pethidine effects could have been due to raised brain tryptophan and 5-HT concentrations.
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PMID:Modification by monoamine oxidase inhibitors of the analgesic, hypothermic and toxic actions of morphine and pethidine in mice. 2 22

The R(-) and S(+)-isomers of 2,5-dimethoxy-4-methylamphetamine (DOM) produce a dose-dependent hypothermia in rats kept in the cold (6 degrees C). 2 This hypothermia was linearly dependent upon ambient temperature and the R(-)-isomer was considerably more potent than the S(+)-isomer. 3 A statistically significant tachyphylaxis was observed when R(-)-DOM was administered on two successive days. The response seven days after the second injection was similar to that on the first day of injection. 4 The hypothermia induced by R(-) and S(+)-DOM was antagonized by methysergide but not by p-chlorophenylalanine (PCPA) or pimozide. Methysergide, PCPA or pimozide alone did not elicit hypothermia at the doses used. The results indicate that R(-) and S(+)-DOM act at post-synaptic 5-hydroxytryptamine receptors.
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PMID:Stereospecific actions of 2,5-dimethoxy-4-methylamphetamine (DOM) on colonic temperature in the rat at various ambient temperatures. 13 54

1. The role of 5-hydroxytryptamine (5-HT) in temperature regulation and in fever in the rabbit has been investigated. 2. Intrahypothalamic microinjections of 5-HT in the conscious rabbit alters body temperature in a dose-dependent manner. 3. Low doses (5-5nmol) of 5-Ht and control saline injections produced a small, non-significant increase in temperature, with a long latency. 4. Doses of 14 nmol 5-HT produce a hyperthermia with a 45 min delay; while microinjections of 28 nmol result in a biphasic response; an initial short hypothermia is followed later by a hyperthermia. 5. Depleting the rabbit's brain of 5-HT by pretreatment with p-chlorophenylalanine (PCPA) fails to affect its body temperature at thermoneutral temperatures but significantly impairs the ability to thermoregulate against a cold stress. 6. PCPA pretreatment did not, however, impair the febrile response to bacterial pyrogen and prostaglandin E1. 7. These results reveal a dissociation between the effects of 5-HT depletion on temperature regulation, and on fever. The site of action of 5-HT in temperature regulation must be proximal to the fever input, but distal to the convengence of peripheral and hypothalamic temperature inputs.
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PMID:A dissociation between temperature regulation and fever in the rabbit. 14 Feb 37

1 The effect of morphine (10 or 20 mg/kg s.c.), pethidine (25 or 50 mg/kg s.c.) or methadone (4 or 8 mg/kg s.c.) on the body temperature of nontreated and p-chlorophenylalanine-pretreated rats was studied at room (21+/-0.2 degrees C) or low ambient (12+/-0.2 degrees C) temperature. 2 Neither pethidine nor smaller doses of morphine and methadone altered the mean rectal temperature of rats kept at room temperature but larger doses of morphine and methadone produced significant hypothermia. 3 All narcotic analgesics at doses used in the present investigation produced significant hypothermia in rats maintained in a low ambient temperature. The hypothermia was prevented by naloxone (1 mg/kg s.c.). 4 The administration of p-chlorophenylalanine (PCPA, 320 mg/kg i.p.) 48 h before the narcotic injection prevented the fall in body temperature both at room and low ambient temperature. 5 The administration of narcotic analgesics at doses, which when administered by themselves did not alter the body temperature of rats, produced significant hyperthermia in rats pretreated with PCPA. 6 When rats pretreated with PCPA were given 5-hydroxytryptophan (75 mg/kg s.c.) 30 min before narcotic administration, the usual response to narcotics was restored. 7 It appears that pethidine and methadone as well as morphine have both hyperthermic and hypothermic actions in rats and that 5-hydroxytryptamine may be involved in the narcotic-induced hypothermia not only at room temperature but also at low ambient temperature.
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PMID:Role of 5-hydroxytryptamine in morphine-, pethidine-, and methadone-induced hypothermia in rats at low ambient and room temperature. 14 36

1. Adenosine 3',5'-monophosphate (cAMP), its dibutyryl derivative (Db-cAMP) and other adenine nucleotides have been micro-injected into the hypothalamic region of the unanaesthetized cat and the effects on body temperature, and on behavioural and autonomic thermoregulatory activities observed. 2. Db-cAMP and cAMP both produced hypothermia when applied to the pre-optic anterior hypothalamus. With Db-cAMP the hypothermia was shown to be dose dependent between 50 and 500 mug (0-096-0-96 mumole). 3. AMP, ADP and ATP also produced hypothermia when injected into the pre-optic anterior hypothalamus. 4. The order of relative potencies of the adenine nucleotides with respect both to the hypothermia produced and to the autonomic thermoregulatory effects observed were similar. Db-cAMP was most potent and cAMP least. 5. Micro-injection into the pre-optic anterior hypothalamus of many substances including saline produced in most cats a non-specific rise in body temperature apparently the result of tissue damage. Intraperitoneal injection of 4-acetamidophenol (paracetamol 50 mg/kg) reduced or abolished this febrile response. 6. The hypothermic effect of the adenine nucleotides has been compared with the effects produced in these same cats by micro-injections of noradrenaline, 5-hydroxytryptamine, a mixture of acetylcholine and physostigmine (1:1), EDTA and excess Ca2+ ions. 7. It is concluded that as Db-cAMP and cAMP both produce hypothermia, it is unlikely that endogenous cAMP in the pre-optic anterior hypothalamus mediates the hyperthermic responses to pyrogens and prostaglandins.
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PMID:The effects of cyclic adenosine 3',5'-monophosphate and other adenine nucleotides on body temperature. 17 Mar 96

Effects of amitriptyline on rectal temperature of male rats were studied at the ambient temperature of 25 degrees C. Drugs were administered intraperitoneally. Amitryptyline elicited a dose related hypothermia. The hypothermia was attenuated by phenoxybenzamine 10 mg/kg, haloperidol 2 mg/kg, diphenhydramine 5 mg/kg, atropine 20 mg/kg, and cyproheptadine 5 mg/kg. Propranolol, at a dose of 5 mg/kg, had no effect on the hypothermia. Theophylline 50 mg/kg and dibutyryl cyclic AMP 20 mg/kg inhibited the hypothermia produced by anitriptyline. Pretreatment with parachloroamphetamine (PCA), 2 or 5 mg/kg daily for 3 days, strongly antagonized the hypothermia. In addition, pretreatment with parachlorophenylalanine (PCPA), 100 mg/kg daily for three days, reduced the brain 5-hydroxytryptamine (5-HT) concentration to 20% of the control level and completely blocked the hypothermia response. When brain 5-HT concentration recovered to 50% of the control level in PCPA treated rats following the administration of 10 mg/kg 5-hydroxytryptophan (5-HTP) the hypothermia induced by amitriptyline was restored. However, the administration of 5-HT, 5 mg/kg, to PCPA treated rats did not increase brain 5-HT concentration or restore the amitriptyline induced hypothermia (AIH). Results suggest that amitriptyline interacts with several transmitter substances to produce hypothermia. Since the ability of amitriptyline to produce hypothermia was correlated with brain 5-HT content, 5-HT might play an important role in the mediation of AIH.
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PMID:Mechanisms of amitriptyline induced hypothermia in the rat. 19 9

The effect of the 5-hydroxytryptamine (5-HT) precursor 5-hydroxytryptophan (5-HTP) on the thermoregulatory responses of unanesthetized rats were assessed at three different ambient temperatures (Ta) of 8, 22 and 31 degrees C. Intraperitoneal administration of either 5-HTP alone or 5-HTP plus R04-4602 (the peripheral decarboxylase inhibitor) produced dose-dependent hypothermia at both Ta's of 8 and 22 degrees C. The hypothermia was brought about solely by a decrease in metabolic heat production at 8 degrees C Ta. At 22 degrees C Ta, the hypothermia was due to both a decrease in metabolic heat production and an increase in tail and footsole skin temperature. However, at 31 degrees C Ta, there were no changes in rectal temperature in response to either 5-HTP or 5-HTP plus R04-4602 application. The data suggest that an increase in 5-HT levels in brain decreases heat production and/or increase heat loss and leads to hypothermia in rats.
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PMID:Elevating serotonin levels in brain with 5-hydroxytryptophan produces hypothermia in rats. 31 May 41

The development of tolerance to delat9-tetrahydrocannabinol (delta9-THC) was examined. Rats with permanently indwelling intravenous catheters were injected daily with delta9-THC, 2 mg/kg, for up to 10 days and on each day subjective behaviour and body weight of each rat were noted. Tolerance appeared to develop to both the excitatory and depressant behavioural effects of delta9-THC, whereas the rate of gain in body weight of delta9-THC treated rats was retarded and tolerance to this phenomenon did not develop over the experimental period. On days 1, 2, 3, 5, 6, and 10 body temperature was recorded continuously for at least 2 h after delta9-THC and in other groups of rats the brain levels of noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) were measured spectrophotofluorimetrically 1 h after delta9-THC. Tolerance developed to the delta9-THC-induced hypothermia by day 3, and on days 6 and 10 hyperthermia was observed. delta9-THC did not markedly affect the brain levels of NA or DA over the experimental period. The brain levels of 5-HT were unchanged on days 1--5 but there was a decrease on days 6 and 10. On days 1, 2, and 3 brain levels of 5-HIAA were raised, whereas on day 6 there was a decrease. These results show that delta9-THC induces tolerance to the hypothermia and elevation of brain 5-HIAA levels in a linear manner. An inverse relationship appears to exist between these two parameters.
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PMID:Relationship between body temperature and brain monoamines during the development of tolerance to delat9-tetrahydrocannabinol in the rat. 41 35


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