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)

1. The effects of intraperitoneal administration of a standard extract of Panax ginseng alone and in combination with morphine were determined in male Sprague-Dawley rats. 2. Ginseng extract at 200 mg/kg produced analgesia and hypothermia. These effects of ginseng were not reversed by naltrexone. 3. A dose of morphine (8 mg/kg) produced analgesia and hyperthermia. The analgesic response to morphine was antagonized by 25 and 50 mg/kg doses of ginseng but not by 12.5, 100 and 200 mg/kg doses. 4. Morphine-induced hyperthermia was antagonized by 12.5-200 mg/kg doses of ginseng. 5. Administration of morphine (50 mg/kg) produced cataleptic effect which was antagonized by 25 mg/kg of ginseng. 6. The results suggest that ginseng extract at high doses produces analgesia and hypothermia in the rat by a non-opiate mechanism, and antagonizes the acute pharmacological effects of morphine.
Gen Pharmacol 1990
PMID:Antagonism of the acute pharmacological actions of morphine by panax ginseng extract. 227 87

The central action of oxaprotiline (OXA) enantiomers, administered in a single dose, was studied in rats and mice. (+)-OXA and (-)-OXA attenuated reserpine- and apomorphine-induced hypothermia [(+)-OXA in a more potent manner] in mice and reduced the immobility time in the behavioural despair test in rats. Both OXA enantiomers inhibited locomotor activity in mice and rats, and enhanced and prolonged amphetamine- and apomorphine-induced stereotypy in rats. (-)-OXA potentiated the amphetamine hyperactivity in rats, but not in mice. Nomifensine hyperactivity in rats was unaffected by either enantiomer, and locomotor hypoactivity induced by low doses of apomorphine was also unchanged, as was L-DOPA-induced locomotor hyperactivity in mice. Apomorphine-induced climbing in mice was attenuated by (+)-OXA. Clonidine locomotor hypoactivity and hypothermia were unchanged, and clonidine-induced aggressiveness was attenuated by (+)-OXA. Neither OXA enantiomer affected the action of oxotremorine. In some tests the effect of OXA was stronger at 3 h than at 1 h after administration. The above results indicate that both OXA enantiomers--in particular (-)-OXA--increase some dopaminergic behavioural effects in rats.
J Neural Transm Gen Sect 1990
PMID:Some central pharmacological effects of (+)- and (-)-oxaprotiline. 231 15

Hypothermic responses to 5-HT1A receptor activation by the selective ligand ipsapirone (IPS) were attenuated in depressed patients as compared to controls. Chronic treatment with amitriptyline (AMI) further impaired 5-HT1A-mediated hypothermia. The results indicate a subsensitive (presynaptic) 5-HT1A receptor and/or a defective post-receptor signalling pathway in depression and are consistent with the hypothesis that 5-HT1A receptors are down-regulated during AMI treatment.
J Neural Transm Gen Sect 1990
PMID:5-HT1A receptor function in depression: effect of chronic amitriptyline treatment. 231 17

The effect of variation in temperature (37-32 and 27 degrees C) on electrical and mechanical activity of depolarized and isoprenaline- or barium-reactivated guinea pig ventricular strips was studied. Lowering the temperature brings a marked prolongation of isoprenaline-induced slow action potentials. In addition the maximal rate of depolarization was strongly reduced at lower temperatures. These effects were observed at an extracellular Ca2+ concentration of either 0.9 or 2.5 mM. The accompanying mechanical activities was significantly increased by reduction in temperature. Barium-induced slow action potentials were similarly affected by temperature variations. These observations suggest that hypothermia exert a sort of calcium antagonistic action probably coupled to a reduction of repolarizing outward potassium currents.
Gen Pharmacol 1986
PMID:Effect of temperature on isoprenaline- and barium-induced slow action potentials in guinea-pig ventricular strips. 243 Aug 55

1. Intraperitoneal (i.p.) injection of diazepam (1.5-6 mg/kg) decreased the core body temperature (BT) of the rats. The effect was dose-dependent. 2. The hypothermia produced by diazepam (6 mg/kg, i.p.) was decreased in animals pretreated with high doses of bicuculline (BIC, 3 mg/kg, i.p.), while low doses of BIC (1.5 mg/kg, i.p.) potentiated the hypothermia. 3. Picrotoxin (PIC, 1 and 2 mg/kg, i.p.) pretreatment also decreased the hypothermic effect of diazepam. 4. Pretreatment of animals with atropine (AT, 10 mg/kg, i.p.) or propranolol (PRO, 10 mg/kg, i.p.) potentiated the hypothermic response of diazepam. Phenoxybenzamine (PHEN, 0.5 mg/kg, i.p.), methergoline (METH, 0.5 mg/kg, i.p.) or pimozide (PIM, 0.5 mg/kg, i.p.) did not change the diazepam hypothermia. 5. Single administration of BIC, PIC, PRO, PIM or METH also induced hypothermia. 6. One can postulate that diazepam hypothermia may be induced through GABAA receptor sites. However, further studies will clarify this hypothesis.
Gen Pharmacol 1989
PMID:Involvement of GABAA receptor sites in diazepam hypothermia. 257 24

1. Intraperitoneal (i.p.) injection of muscimol (MUS, 2-8 mg kg-1) decreased the core body temperature (BT) of the rats dose-dependently. 2. Intracerebroventricular (i.c.v.) injection of MUS (1 microgram/microliter/rat) also caused a fall in BT. 3. The hypothermia induced by MUS was inhibited by pretreatment of the animals with either bicuculline (BIC) or picrotoxin (PIC). 4. i.p. Injection of baclofen (BAC, 2.5-10 mg kg-1) induced hypothermia. Higher dose of the drug (20 mg kg-1) caused an initial fall followed by a marked increase in BT. 5. i.c.v. Injection of BAC produced a rise in BT. 6. The hypothermic effect of BAC was antagonized in animals pretreated with either BIC or PIC, while hyperthermic effect of the drug was potentiated with PIC pretreatment. 7. i.c.v. Injection of isoguvacine (ISO) induced hypothermia, which was attenuated in rats pretreated with either BIC or PIC. 8. It can be concluded that: activation of GABAA or GABAB receptor sites respectively may induce hypothermia or hyperthermia in rats.
Gen Pharmacol 1988
PMID:GABAA and GABAB receptor sites involvement in rat thermoregulation. 283 45

The effects of gamma-aminobutyric acid (GABA) on body temperature of restrained rats has been studied. GABA (250-1000 mg/kg i.p.) caused a dose-dependent fall in BT of restrained rats at an ambient temperature of 18-22 degrees C. The GABA-induced hypothermic response was attenuated by pretreatment with hexamethonium, p-chlorophenylalanine, methysergide, neostigmine and atropine (% MPE values: 27, 35, 51, 64 and 72 respectively). Pretreatment with methysergide and atropine was more potent than hexamethonium and methysergide in inhibiting the GABA-induced hypothermia (% MPE = 68 and 47 respectively). The antagonism by neostigmine of GABA-induced hypothermia was attenuated by pretreatment with hexamethonium (7.5 mg/kg). Yohimbine and chlorimipramine potentiated GABA hypothermia (% MPE = -82 and -8 respectively). The data indicate that GABA-induced hypothermia may be mediated by serotonin and acetylcholine release. Muscarinic receptors may play an important role in the effect of GABA. The results support the hypothesis that the hypothermia induced by GABA is modulated by nicotinic receptors.
Gen Pharmacol 1986
PMID:GABA-induced hypothermia in rats: involvement of serotonergic and cholinergic mechanisms. 294 36

GABA, delta-aminovaleric acid (DAVA) and sodium valproate (VPA) decrease core temperature in conscious rats. Bicuculline increases GABA-induced hypothermia, does not modify DAVA (250 mg/kg) and VPA (100 and 400 mg/kg) hypothermia and antagonizes initial hypothermia by DAVA (1000 mg/kg) and VPA (200 mg/kg) and late hypothermia by DAVA (500 mg/kg) and VPA (200 mg/kg). Picrotoxin increases late hypothermia by GABA (250 mg/kg) and VPA (400 mg/kg), but decreases initial hypothermia by VPA (200 mg/kg). Pentylenetetrazol increases variably GABA-induced hypothermia, inhibits early early hypothermia by DAVA and increases hypothermia induced by VPA (400 mg/kg). We conclude that GABA and GABA-agonists (DAVA and VPA) may induce hypothermia partly mediated by activation of bicuculline-insensitive GABA-receptors.
Gen Pharmacol 1985
PMID:Involvement of bicuculline-insensitive receptors in the hypothermic effect of GABA and its agonists. 299 72

Nifedipine exhibits a greater incidence of side effects than the other currently marketed calcium channel antagonists. In addition to those effects attributable to calcium channel blockade, nifedipine produces side effects similar to the effects of adenosine. It is probable that nifedipine exerts part of its physiological actions through potentiation of adenosine. Adenosine, an endogenous calcium channel blocker, modifies synaptic events throughout the nervous system and causes sedation, smooth and skeletal muscle relaxation, anticonvulsion, hypotension and hypothermia, all reversible by caffeine or theophylline administration. Nifedipine inhibits adenosine uptake from, and release into, the extracellular space and binds at an adenosine receptor. Both nifedipine and adenosine interact with benzodiazepine binding sites. Interaction between nifedipine and adenosine should be kept in mind when treating patients with nifedipine.
Gen Pharmacol 1986
PMID:Nifedipine: more than a calcium channel blocker. 301 14

Morphine (30 mg/kg i.p.) produced a hypothermic effect in restrained rats which was antagonized by naloxone pretreatment (10 mg/kg s.c.). This hypothermia was inhibited by deprenyl pretreatment (5 mg/kg i.p.) and by beta-phenylethylamine treatment (25 mg/kg i.p.). However, the effect of morphine was partially potentiated when a higher dose of deprenyl (10 mg/kg i.p.) was administered. Pretreatment with clorgyline (1 mg/kg i.p.) potentiated the morphine-induced hypothermia. In contrast, the effect of morphine was antagonized when a higher dose of clorgyline was used (5 mg/kg i.p.). Based on these results, a possible role of brain serotonin and dopamine in the thermoregulatory effects of morphine is proposed in this paper.
Gen Pharmacol 1987
PMID:Effect of selective monoamine oxidase inhibitors on the morphine-induced hypothermia in restrained rats. 310 35


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