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

Rats were rendered tolerant to ethanol by daily gavage of 4--5 g/kg. The degree of motor impairment on the moving belt test and of hypothermia after i.p. test doses of ethanol was measured prior to and at various times during the chronic treatment, to assess the rates of tolerance development. L-Tryptophan (75 mg/kg twice daily) was administered chronically to elevate brain serotonin level. This treatment did not alter the motor impairment or hypothermia produced by the initial test doses of ethanol (2.0 and 2.5 g/kg respectively). However, the development of tolerance to both the motor impairment and hypothermia effects of ethanol was accelerated in the tryptophan-treated rats. This finding complements our earlier observations that depletion of 5-HT with p-CPA slows down tolerance. Blood ethanol measurements at 20 min (motor impairment) or 90 min (hypothermia) after the administration of the test dose reveal no significant difference between the control and tryptophan-treated rats, suggesting that tryptophan did not influence the metabolism of ethanol. This finding supports the hypothesis that brain serotonin modulates the development of tolerance to ethanol.
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PMID:Effect of L-tryptophan on the acquisition of tolerance to ethanol-induced motor impairment and hypothermia. 10 29

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

The mixed 5-hydroxytryptamine1A (5-HT1A) receptor agonist/antagonist 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspirol-[4.5]- decane-7,9-dione (BMY 7378) (5 mg/kg) did not significantly depress body temperature, but pretreatment with BMY 7378 blocked hypothermia induced by the selective 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). In contrast, another partial 5-HT1A agonist, pindolol (10 mg/kg), slightly but significantly depressed body temperature by itself but did not attenuate hypothermia elicited by 8-OH-DPAT. Attempts to identify the synaptic locus of the receptor were unsuccessful because depletion of central serotonin (5-HT) by treatment with para-chlorophenylalanine (PCPA; 3 x 150 mg/kg) did not alter the hypothermic response to 8-OH-DPAT. Partial, irreversible 5-HT1A receptor inactivation by N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) (1 mg/kg) reduced the maximal hypothermic effect of 8-OH-DPAT (to 53% of control) without altering its ED50 (0.96 mg/kg). Analysis of the data indicated a linear relationship between 5-HT1A receptor occupancy and hypothermic response, that is, absence of receptor reserve. When groups of mice were treated with each of five different doses of 8-OH-DPAT (0.04, 0.16, 0.63, 2.5, and 10 mg/kg) 48 h apart, there was a significant reduction in hypothermic response after the second injection, but only at the three highest doses. The results demonstrate that 8-OH-DPAT-induced hypothermia in mice is mediated by a 5-HT1A receptor whose synaptic localization is uncertain but that has no receptor reserve. In addition, tolerance is observed after only a single agonist treatment.
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PMID:Serotonin 5-HT1A receptor-mediated hypothermia in mice: absence of spare receptors and rapid induction of tolerance. 135 73

We have examined the effects on sleep and brain temperature of bilateral microinjections of adenosine and adenosine analogs to the preoptic area (PO) of rats. Administration of adenosine (12.5 nmoles), a nonselective adenosine A1/A2 receptor agonist NECA (N-ethyl-carboxamido-adenosine, 1.0 nmole), and the selective adenosine A1 receptor agonist CPA (cyclopentyladenosine, 0.25, 0.5 nmoles) increased total sleep primarily through an enhancement in deep slow-wave sleep (SWS2), while adenosine also increased REM sleep. Administration of 12.5 nmoles adenosine and 0.25 nmoles CPA did not affect brain temperature, while 1.0 nmole NECA and 0.5 nmoles CPA caused a transient and prolonged hypothermia, respectively. Administration of the selective adenosine A2 receptor agonist CV-1808 (2-phenylaminoadenosine, 5, 10 nmoles) had no effect on sleep or brain temperature. The present results demonstrate a site for the central hypnotic action of adenosine, and a functional role for adenosine A1 receptors in the hypothalamus.
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PMID:Role of adenosine in sleep and temperature regulation in the preoptic area of rats. 178 Mar 43

The rectal temperature and serum corticosterone increased in mice exposed to 45 degrees C for 15 min; at the same time, the contents of brain 5-HT and NE reduced, brain DA unchanged. Ginseng root saponins (GRS) ip 200 mg/kg inhibited the increase of serum corticosterone and the decrease of brain 5-HT and NE in heat-stressed mice, but did not affect brain DA. GRS lowered mice body temperature at room temperature and inhibited the rise of body temperature under heat environmental conditions in mice. Reserpine eliminated the hypothermia of GRS at room temperature and its inhibitory effect on hyperthermia under heat-stress conditions. PCPA eliminated only the inhibition of GRS on hyperthermia under heat-stress, but had no significant effect on hypothermia at room temperature.
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PMID:Effects of ginseng root saponins on brain monoamines and serum corticosterone in heat-stressed mice. 264 45

Since we have previously observed a genetic difference in the development of tolerance to the narcotic effect of ethanol in UChA and UChB rats when providing them with a 10% v/v ethanol solution as sole drinking fluid, experiments were performed in order to know whether the resistance to development of tolerance to ethanol in UChB rats was also exhibited after other regimens of ethanol administration, namely, a 2.76 g/kg ethanol IP injection 24 hr before the experiment, only 10% v/v ethanol solution as sole drinking fluid for 21 days, or receiving acutely a daily dose of 2.76 g/kg ethanol by gavage for seven days. Participation of serotoninergic neurons was tested by treating rats with p-chlorophenylalanine (p-CPA), a known serotonin depletor. Results show that UChA rats developed tolerance to ethanol-induced narcosis and hypothermia, while UChB rats developed it to narcosis only when they received acute oral doses of ethanol for 7 days and did not develop tolerance to hypothermia with any of the treatment regimens. p-CPA pretreatment did prevent the development of tolerance in both strains of rats, confirming the participation of serotoninergic neurons in ethanol tolerance in rats.
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PMID:Effect of different treatment regimens with ethanol and p-chlorophenylalanine on tolerance development in UChA and UChB rats. 297 92

The potent, centrally acting 5-HT receptor agonist 8-OH-DPAT was shown to induce a clearcut hypothermic response in naive and PCPA-pretreated conscious rats, maintained at 22 degrees C. PCPA pretreatment decreased the threshold dose of 8-OH-DPAT required to cause hypothermia, indicating that a sensitisation of 5-HT-receptor dependent mechanisms was involved. The results are discussed with reference to recent 5-HT receptor subclassification. It is suggested that body temperature measurements in the rat might provide a simple in vivo physiological means of studying central serotoninergic mechanisms, including 5-HT receptor sensitivity modification.
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PMID:Hypothermia in the rat induced by the potent serotoninergic agent 8-OH-DPAT. 315 65

p-Chlorophenylalanine (p-CPA) reduces brain 5-hydroxytryptamine (5-HT) without altering the dopamine and norepinephrine content. Morphine does not influence the 5-HT level, but partly reverses the depletion of 5-HT by p-CPA. Morphine analgesia and toxicity are not affected by p-CPA treatment. p-CPA also has no effect on acute morphine hypothermia, but after chronic treatment of 5-HT-deficient mice the dose--response curve is no longer parallel, which suggests that another mode of morphine hypothermia occurs. p-CPA diminishes morphine-induced running after acute as well as after chronic morphine administration. p-CPA treatment reduces the sensitivity to the naloxone-precipitated withdrawal reaction, but does not affect the development of physical dependence.
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PMID:The influence of p-chlorophenylalanine on different morphine effects. 644 58

Previously it has been shown that chronic administration of p-chlorophenylalanine (p-CPA), slowed the development of tolerance to ethanol, pentobarbital and cross-tolerance development to ethanol in rats chronically treated with pentobarbital. These findings have been extended by the following observations: (1) p-CPA slowed the development of tolerance to barbital as measured by motor impairment on the moving belt test, without altering the acute response. (2) p-CPA also reduced the tolerance to barbital as measured by sleeping time, in animals chronically treated with pentobarbital. (3) Administration of L-tryptophan increased the rate of tolerance development to ethanol as measured by motor impairment and hypothermia. These results further confirm and extend the generality of our observations that 5-HT may be involved in the development of tolerance and cross-tolerance to sedatives.
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PMID:Role of serotonin (5-HT) in tolerance to ethanol and barbiturates. 644 35

Immobilization of albino rats for 2 h showed ambient temperature-dependent changes in rectal temperature, hypothermia at temperatures below 30 degrees C, and hyperthermia at 35 degrees C and above. Adrenalectomized (Adre) rats showed more hypothermia compared to sham operated controls at 25 +/- 2 degrees C. The increased hypothermia in adrenalectomized rats was reversed by 10 mg/kg IP or 100 microgram/rat ICV of hydrocortisone. Groups of rats pretreated with desmethylimipramine (DMI, 25 mg/kg IP) and 6-hydroxydopamine (6-HD, 100 microgram/rat ICV) or methyl ester of parachlorophenylalanine (ME-PCPA, 100 microgram/rat ICV for 3 days) or 5,6-dihydroxytryptamine (DHT, 75 microgram/rat ICV) showed significantly less hypothermia at the end of 2 h of immobilization. Applying analysis of variance test, the hypothermia in Adre, ME-PCPA and DHT groups, was found to be not significantly different from their respective control groups between 0 and 45 min of immobilization but was significantly different between 45 to 120 min of immobilization. DMI-6-HD group however, showed significant difference between 0--45 min only and not between 45--120 min of immobilization. The results suggest that the early phase of immobilization induced hypothermia between 0--45 min is dopamine and the late phase of hypothermia between 45--120 min is 5-hydroxytryptamine mediated.
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PMID:Immobilization stress in rats: effect on rectal temperature and possible role of brain monoamines in hypothermia. 645 54


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