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

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

The action of copper (CuSO4, 5 mg/kg, oral) on selected neuropharmacological actions of cannabis resin (CI, oral) was studied on albino rats and mice. Copper potentiated the barbiturate hypnosis-potentiating activity of CI in albino rats and mice and had no effect on hypothermic activity in albino rats. Single doses of copper partially inhibited tolerance to barbiturate hypnosis-potentiation activity and markedly delayed the development of tolerance to hypothermic activity of CI. Oral as well as i.c.v. copper (CuSO4, 0.1 microgram) in single dose antagonised the tolerance to hypothermic activity of cannabis or THC for one to two weeks. Copper-CI interaction could be antagonised by penicillamine. Zinc (ZnSO4, 5 mg/kg, oral) had an action similar to that of copper in antagonising the development of tolerance to the hypothermic activity of CI, but magnesium (MgSO4, 5 mg/kg, i.p.) was devoid of any such action. Studies indicate that, although copper has no significant neuropharmacological action, it interacts with CI activity, especially in tolerant rats, in effects on hypothermia. The site of action of copper is possibly the hypothalamus, where it inhibits the processes of tolerance development to CI on the noradrenergic neurone.
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PMID:Studies on the interactions of copper and cannabis. 41 40

Tetrabenazine evoked a biphasic response in rectal temperature of the rat following intraperitoneal administration of 4.4--70.0 mg/kg. The initial hyperthermia was inversely related to the dose while the subsequent hypothermia was dose-dependent. This biphasic effect on temperature was similar to that seen with THC at 0.5 mg/kg, thus adding further evidence of a similarity in the mode of action of the two drugs. In contrast, only hypothermia was evident following chlorpromazine administration.
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PMID:Comparative effects of delta 9-tetrahydrocannabinol, tetrabenazine and chlorpromazine on rectal temperature in the rat. 48 45

The effects of i.v. injected delta9-tetrahydrocannabinol (delta9-THC) on behaviour, body temperature and levels of brain monoamines, measured spectrophotofluorimetrically, of the rat were determined. Doses of delta9-THC in the range of 0.05--5.0 mg/kg produced biphasic changes in behaviour, body temperature and levels of 5-hydroxyindoleacetic acid (5-HIAA). The whole brain levels of dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) were not altered by delta9-THC. The subjective behavioural biphasic responses did not appear to be dose related, whereas the biphasic changes in body temperature and brain levels of 5-HIAA were dose-related. Low doses of delta9-THC (0.05 and 0.1 mg/kg) caused hyperthermia, while doses of 1.0, 2.0 and 5.0 mg/kg induced hypothermia. On the other hand, 0.05 mg/kg delta9-THC significantly reduced, whereas doses of 1.0, 2.0 and 5.0 mg/kg significantly increased the 5-HIAA levels in a dose-related manner. It is concluded that an inverse relationship exists between delta9-THC-induced changes in body temperature and alterations in brain 5-HIAA levels.
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PMID:Biphasic nature of the effects of delta9-tetrahydrocannabinol on body temperature and brain amines of the rat. 59 Mar 30

Rats pretreated daily with delta9-tetrahydrocannabinol (delta9-THC, 8 mg/kg) during 14 days showed tolerance to THC-induced hypothermia and depression of CAR acquisition in a shuttle-box. The noncontingent exposure of THC also produced tolerance to spontaneous (unlearned) behaviors as measured in a open-field test. The data suggest no essential role for learned tolerance in the sense that animals have to to learn to perform under the influence of THC for several of these behaviors.
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PMID:delta9-Tetrahydrocannabinol: tolerance after noncontingent exposure in rats. 63 25

1 The effect of pretreatment with clomipramine hydrochloride (15 mg/kg, i.p.) on the (--)-trans-delta9-tetrahydrocannabinol (delta9-THC)-induced changes in body temperature and brain amines of the rat was investigated. 2 A dose of 0.05 mg/kg of delta9-THC produced hyperthermia and a decrease in whole brain concentration of 5-hydroxyindoleacetic acid (5-HIAA). Doses of 2 and 5 mg/kg produced hypothermia and increases in brain 5-HIAA whereas 0.5 mg/kg did not affect either parameter. delta9-THC, at any of the doses, did not affect the whole brain concentrations of dopamine, noradrenaline or 5-hydroxytryptamine. 3 Clomipramine modified these responses of delta9-THC in that the dose-response curves appeared to be shifted to the right. 4 It is concluded that clomipramine acts as an antagonist to these actions of delta9-THC by interfering with entry of delta9-THC into tryptaminergic neurones.
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PMID:Antagonism of the effects on thermoregulation of delta9-tetrahydrocannabinol by clomipramine in the rat. 66 19

delta9-Tetrahydrocannabinol (THC; 2.5, 5.0, 10.0 mg/kg, PO) impaired avoidance and rotarod performance, and caused bradycardia and hypothermia. Phencyclidine (PCP; 1.25, 2.5, 5.0 mg/kg, IP) impaired avoidance and rotarod performance and caused a marked increase in photocell activity. When combined, the depressant properties of each drug were enhanced and the stimulation of photocell activity cg/kg THC and its interactions with PCP followed subacute treatment for six days, whereas many of the effects of PCP were enhanced after subacute treatment with a dose of 2.5 mg/kg. Open-field behavior was affected by each drug alone and in combination in a similar way as photocell activity, but the depression caused by their interaction was greater; both drugs caused an increase in urination. Response rates on an FR-10 schedule of food reinforcement were decreased by 2.5 mg/kg PCP, but not by 5.0 mg/kg THC; the combination caused greater response suppression than either drug alone. The functional interactions between THC and PCP were not related to changes in the concentrations of 14C or 3H in plasma or brain derived from 14C-delta9-THC and 3H-PCP, respectively.
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PMID:Interactions between delta9-tetrahydrocannabinol and phencyclidine hydrochloride in rats. 85 Jun 86

1. Rats were injected intravenously with 2 mg/kg (-)-trans-delta9-tetrahydrocannabinol (delta9-THC) at ambient temperatures of 4 degrees, 21 degrees, 31 degrees and 37 degrees C. 2. The general behavior exhibited by rats treated with delta9-THC was similar at all four ambient temperatures. 3. Body temperatures were recorded continuously before and after drug administration. At 4 degrees and 21 degrees C, delta9-THC caused hypothermia whereas no change in body temperature occurred at 31 degrees and 37 degrees C. 4. The concentrations in the whole brain of noradrenaline (NA), dopamine, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were determined spectrophotofluorimetrically 1 h after drug administration. At 4 degrees C delta9-THC caused an increase of 5-HT, at 21 degrees C an increase of 5-HIAA, at 21 degrees C an increase of 5-HIAA AND A decrease of NA, and at 37 degrees C an increase of 5-HT and 5-HIAA. 5. At all ambient temperatures, delta9-THC increased the brain levels of 5-HT and/or 5-HIAA. A correlation between the delta9-THC-induced hypothermic response and the possible alteration of brain 5-HT metabolism cannot be excluded.
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PMID:The effect of delta9-tetrahydrocannabinol on body temperature and brain amine concentrations in the rat at differnt ambient temperatures. 88 91

1. Experiments with untreated mice confirmed that at ambient temperatures below 30 degrees C, the oxygen consumption rate of mice normally kept at about 23 degrees C varies inversely with ambient temperature. 2. At given ambient temperatures in the range 20 to 31 degrees C the oxygen consumption rate was 32 to 43% greater for restrained than for unrestrained mice. 3. Hypothermia induced in restrained mice by delta9-tetrahydrocannabinol (delta9-THC) (1.0 to 4.0 mg/kg i.v.) was accompanied by marked falls in the rate of oxygen consumption. The size of these falls parallelled the degree of hypothermia and increased both with increases in dose and with decreases in the ambient temperature. The oxygen consumption rates of unrestrained mice were also lowered by hypothermic doses (10 to 40 mg/kg i.p.) of delta9-THC. 4. The maximum falls in oxygen consumption rate occurred at earlier times after drug administration than the maximum falls in rectal temperature. 5. At none of the ambient temperatures studied did the oxygen consumption rates of delta9-THC-treated mice fall significantly below the basal levels (59 +/- 3 ml 25 g-1 h-1) of unrestrained, resting mice at 30 degrees C. 6. The hypothesis that reduced rates of heat production contribute significantly towards the hypothermia induced by delta9-THC in our experiments is discussed. The possibility that biological processes responsible for increased heat production in response to cold are more sensitive to delta9-THC than those processes governing basal rates of heat production at thermally neutral environmental temperature is also raised.
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PMID:Effects of delta9-tetrahydrocannabinol on the rates of oxygen consumption of mice. 90 69

The tetrahydrocannabinols are among the most potent hypothermic agents known. A comparison of the hypothermic action of delta9-tetrahydrocannabinol (delta9-THC) with chlorpromazine (CPZ) and morphine shows the following order of hypothermic potency: CPZ greater than delta9-THC greater than morphine. A marked depression of oxygen consumption is produced by delta9-THC both in vivo and in the isolated perfused liver preparation. Simultaneous measurement of core temperature and tail temperature after delta9-THC shows that tail temperature is decreased more by delta9-THC than it is in animals that attain comparable core hypothermia without drug treatment. From these results, it is concluded that delta9-THC-induced hypothermia results primarily from decreased heat production and not from increased heat loss. Therefore, the processes involved in the hypothermic response to delta9-THC appear to differ from those that mediate CPZ- or morphine-induced hypothermia. A hypothesis is discussed in which the hypothermic action of delta9-THC is related to inhibition of membrane ATPase.
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PMID:Profound hypothermia in mammals treated with tetrahydrocannabinols, morphine, or chlorpromazine. 91 17


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