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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 6 benzamides and 8 classical neuroleptics were studied on 6 different apomorphine-induced effects. These drugs did not antagonize all the effects in the same way. The differences are discussed according to the two types of dopaminergic receptor hypothesis. Some apomorphine-induced effects (stereotyped behavior, circling behavior, climbing behavior, and increased motor activity) could be related to stimulation of one type of dopaminergic receptor, other effects (hypothermia and decreased activity) to the other type. Pimozide, sulpiride, thioproperazine, GRI 1665 and TER 1546, could block selectively one type of dopaminergic receptor, at least in a given range of doses. Clozapine, chlorpromazine, levomepromazine, and thioridazine, could block selectively the other type of dopaminergic receptor. Haloperidol, metoclopramide, prochlorperazine, sultopride, and tiapride, could block both types of dopaminergic receptors with equal intensity whatever the dose.
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PMID:Benzamides and classical neuroleptics: comparison of their actions using 6 apomorphine-induced effects. 2 58

In mice, both apomorphine and pilocarpine either potentiated a hypothermic effect of a high dose of morphine or reversed a hyperthermic effect of a low dose of morphine to a hypothermic effect. Haloperidol paritally blocked the hypothermic effect but not the hyperthermic effect of morphine. Scopolamine partially blocked the hyperthermic but not the hypothermic effect of morphine. Bilateral lesions of the caudate nuclei produced no changes in sensitivity to either the acute hyperthermic or hypothermic effect of morphine but did selectively facilitate the developement of tolerance to morphine-induced hypothermia. The results suggest that morphine's temperature effects are determined by the interaction of several mechanisms and that the caudate nucleus may have a specific role in drug tolerance.
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PMID:Hyperthermic and hypothermic effects of morphine in mice: interactions with apomorphine and pilocarpine and changes in sensitivity after caudate nucleus lesions. 114 21

Changes in rectal and skin temperatures following intraventricular injection of biogenic amines and related substances were investigated in rats. Intraventricular injection of norepinephrine in a small dose (6 mug) produced a slight elevation of rectal temperature, but in larger amounts (25-50 mug) resulted in a dose-dependent hypothermia which was associated with a marked rise of skin temperature. No change was observed in plasma free fatty acid and glucose levels and oxygen consumption after intraventricular injection of norepinephrine (25 mug). Intraventricular injection of imipramine and safrazine produced a slight fall in the rectal temperature. Norepinephrine-induced hypothermia was more pronounced in rats pretreated with safrazine and less in rats pretreated with alpha-methyl-p-tyrosine, as compared with that in controls. Intraventricular injection of 6-hydroxydopamine (0.75-250 mug) brought about a marked dose-dependent hypothermia. The second injection of 6-hydroxydopamine 5 days after the first injection had no effect on the body temperature. Norepinephrine injection 2 days after the second injection of 6-hydroxydopamine produced a more pronounced hypothermia than the change in control rats without pretreatments. Haloperidol did not affect the hypothermia induced by 6-hydroxydopamine. Intraventricular injection of dopamine and L-DOPA showed less effect that norepinephrine had. Intraventricular injection of phenoxybenzamine prior to norepinephrine blocked the hypothermia and skin temperature elevation which are normally observed following norepinephrine injection, while propranolol given in the same way showed less or no effect. Intraventricular injection of phenylephrine produced a dose-dependent hypothermia, whereas no dose-response relationship was obtained by isoproterenol. These results suggest that in the rat the hypothermic effect of norepinephrine injected intraventricularly is mediated by an action of central alpha-receptor. At high and low ambient temperatures hypothermia was similarly observed following intraventricular injection of 5-hydroxytryptamine (25 mug) as at normal room temperature. On the other hand, norepinephrine (25 mug) produced a rise in rectal temperature at high ambient temperature and a marked fall at low ambient temperature. The hypothermic effect of norepinephrine was not different between cold-adapted ones at room temperature. From the results the role of norepinephrine and other biogenic amines in the brain in thermoregulatory processes was discussed.
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PMID:[Role of brain biogenic amines in the central thermoregulatory mechanism of the rat (author's transl)]. 124 80

Intracerebroventricularly administered dopamine produced dose dependent hyperthermia in rabbits. Haloperidol, a D1 receptor blocker produced consistent hypothermia, whereas D2 receptor blocker metoclopramide produced hyperthermia, pretreatment with haloperidol competitively blocked the hyperthermic response of dopamine. Pretreatment with metoclopramide augmented the onset and peak response of dopamine. It is suggested that D1 receptors are involved in producing hyperthermia and D2 receptors in hypothermia.
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PMID:Characterization of dopamine receptors involved in central thermoregulation in rabbits. 181 89

GK 13 (N-[1-(2-benzo (b) thiophenyl)-cyclohexyl] piperidine), GBR 12783 (1-[2-(diphenylmethoxy)-ethyl] 4-(3-phenyl propenyl)-piperazine and dexamphetamine are three indirect catecholaminergic agonists, acting via different neurochemical mechanisms. We have compared their effects in rodents, in several behavioral tests. All three drugs increased locomotion. The stimulant locomotor effect of dexamphetamine was more easily antagonized by haloperidol than that of GBR 12783 and GK 13. Only dexamphetamine reversed reserpine-induced akinesia. This reversal was prevented by pretreatment with either GK 13 or GBR 12783. The three drugs reduced pentobarbital sleeping time in mice. They induced rotation ipsilateral to a unilateral 6-OHDA lesion of the nigrostriatal dopaminergic pathway. The stereotypies induced by GK 13 and GBR 12783 were essentially limited to sniffing. Haloperidol-induced catalepsy was apparently more easily antagonized by dexamphetamine than by GK 13 or GBR 12783. GK 13 and GBR 12783 had no significant effects on body temperature. The three drugs displayed an anti-immobility effect in the "despair test". Dexamphetamine and GK 13 reversed the hypothermia induced by apomorphine (16 mg/kg), as well as reserpine-induced hypothermia and reserpine-induced ptosis. Dexamphetamine induced a dose-dependent anorectic effect, whereas GK 13 and GBR 12783 induced only a brief and partial anorexia. Similar observations were made on water intake. Pretreatment with either GBR 12783 or GK 13 did not affect the dexamphetamine-induced anorexia. Effects of the three drugs are discussed by reference to their known neurochemical properties on catecholaminergic transmission.
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PMID:Comparison of the effects of three indirect dopamine agonists, GK 13, GBR 12783 and dexamphetamine on behavioural tests involving central catecholaminergic transmissions. 197 95

The effect of nicotine on the neuroleptic-induced changes in striatal dopamine (DA) metabolism of mice was studied. To investigate the mechanism of action of nicotine, its interactions with apomorphine (APO) and gamma-hydroxybutyric acid (GHBA) were also investigated. Mice were given nicotine, (0.3-3 mg/kg subcutaneously) repeatedly (4 times) at 30 min. intervals. Haloperidol (HAL), (+/-)-sulpiride (SUL), APO or GHBA were administered after the second nicotine dose. Hexamethonium was given to prevent the effects of nicotine on autonomic ganglia. The striatal contents of DA and of its metabolites homovanillic acid (HVA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) were measured. The drug-induced hypothermia in mice was controlled by increasing ambient temperature. At ambient temperature of 32-34 degrees nicotine and HAL increased the striatal DOPAC and HVA contents additively, whereas APO counteracted the effects of nicotine at this ambient temperature. At 20-22 degrees nicotine decreased the 3-MT content which indicates reduced release of DA. In hypothermic mice nicotine inhibited better the HAL- and SUL-induced increases of HVA content than those of DOPAC content suggesting that the neuroleptic-induced increases in DOPAC and HVA contents are mediated partly by different mechanisms. In APO-treated mice both the GHBA- and nicotine-induced decreases of 3-MT content fell further. GHBA did not alter the nicotine-induced decrease of 3-MT content and so this effect of nicotine may be mediated indirectly via GABAergic neurones. Unlike GHBA and APO nicotine decreased 3-MT content only in hypothermic mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dual effects of nicotine on neuroleptic-induced changes of striatal dopamine metabolism in mice. 256 30

In these experiments representative selective antagonists at D1 (SCH 23390) and D2 (haloperidol) receptors were studied for their effects on basal and apomorphine decreased body temperature in mice and rats. In mice, SCH 23390 (up to 3 mg/kg SC) neither affected basal body temperature nor blocked apomorphine-induced hypothermia (AIH). On the other hand, haloperidol alone was hypothermic and paradoxically also blocked AIH in mice. In rats, SCH 23390 alone produced hyperthermia; the mechanism by which this occurred is not known. SCH 23390 also blocked AIH in rats. However, the inhibition of AIH only occurred at doses of SCH 23390 that were themselves hyperthermic. Haloperidol did not alter basal body temperature but did block AIH in rats. These data suggest that apomorphine-induced body temperature changes are D2 mediated.
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PMID:Effects of D1 and D2 antagonists on basal and apomorphine decreased body temperature in mice and rats. 297 95

Previously it was found that during the loss of postural support induced by combined administration of haloperidol and morphine, rats became markedly hypothermic. The present work was a more detailed study of this hypothermia. Morphine alone (20 mg/kg) produced a slight hyperthermia (1 degrees C) in female rats and no effect in males. Haloperidol alone (5 mg/kg) elicited a hypothermia of about 3 degrees C in females and no effect in males. The combination of both elicited a greater decrease of temperature (about 5 degrees C) in female rats and, unexpectedly, a decrease of 3 degrees C in males. According to these data, increased endorphinic activity with a concomitant decrease in dopamine in some unidentified regions of the central nervous system causes hypothermia.
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PMID:Sex differences in the effects of haloperidol, morphine, and their combination on colonic temperature in rats. 356 61

General pharmacological properties of 4'-fluoro-4-[4-(2-thioxo-1-benzimidazolinyl) piperidino] butyrophenone (timiperone), a new neuroleptic drug, were compared with those of haloperidol. 1. Central nervous system: In behavioral observation, timiperone showed a typical neuroleptic profile at doses of 0.1 mg/kg p.o. and more (mice). The drug produced a moderate hypothermia at 10 mg/kg p.o. (rabbits), a mild increase in pain threshold at 3 mg/kg p.o. (mice and rats) and a slowing of cortical EEG at 1 mg/kg i.v. (cats). ED50 values of drug for the potentiation of ether and alcohol anesthesia were 0.34 and 0.22 mg/kg p.o., respectively (mice). Timiperone ahd neither an anticonvulsant activity at 30 mg/kg p.o. (mice) nor an effect on the spinal reflex at 1 mg/kg i.v. (cats). These effects of timiperone on the central nervous system were almost similar to those of haloperidol. 2. Respiratory and cardiovascular system: At dose of 0.03 mg/kg i.v. and more, timiperone produced transient increases in respiratory rate and regional arterial blood flow which were accompanied by a fall in blood pressure (dogs). Haloperidol had qualitatively similar effect, but was weaker than timiperone. Both drugs at high concentration (3X10-6 g/ml) exerted negative inotropic and chronotropic effect in isolated atrial preparations (guinea-pigs), and non-competitively antagonized the positive chronotropic action of isoprenaline. Atropine (2.5X10-7 g/ml) failed to modify the chronotropic action of timiperone (3X10-6 g/ml). 3. Autonomic nervous system: Timiperone at 0.1 mg/kg p.o. and haloperidol at 0.3 mg/kg p.o. induced a moderate miosis (rabbits) and antagonized blood responses to noradrenaline and acetylcholine (dogs). Both drugs at 1 mg/kg i.v. had no ganglion-blocking activity (cats). 4. Smooth muscle: In isolated guinea-pig ileum and vas deferens, timiperone and haloperidol (10-5 g/ml) antagonized the contractile responses of the muscles to various spasmogens, Both drugs at approximately 10-6 g/ml decreased spontaneous motility of the isolated rat uterus and inhibited the gastric secretion at 1 mg/kg i.p. (rats). At high doses, both drugs inhibited the gastrointestinal propulsion (mice), motility (dogs) and gastric emptying rate (rats), and had no damaging effect on the gastric mucosa (rats). 5. Skeletal muscle: At 0.1 mg/kg i.v., timiperone and haloperidol slightly enhanced twitch response of the anterior tibial muscle to electrical stimulation (rabbits). 6. Urine volume and urinary electrolytes: Timiperone and haloperidol showed a diuretic effect at 3 mg/kg p.o. whereas they inhibited urine output and electrolytes excretion at 30 mg/kg p.o. (rats).
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PMID:Pharmacological studies on timiperone, a new neuroleptic drug Part II: General pharmacological properties. 611 34

To clarify the impact of hypothermia on the hormonal control of glucose metabolism, rats were rendered hypothermic (25 C) after catheterization of the portal vein. Glucose, insulin, glucagon, and catecholamine concentrations were serially monitored, and the regional blood flows were measured, allowing the estimation of hormone outputs. Hypothermia reduced the portal blood flow by 50% without changing arterial blood pressure, blood gases, or pH. Portal plasma insulin secretion dropped (0.05 +/- 0.01 vs. 0.23 +/- 0.04 mU/min), and glucagon secretion increased (0.81 +/- 0.18 vs. 0.38 +/- 0.10 ng/min). The B cell responses to glucose, arginine, and glucagon were abolished, while the A cell response to arginine was not significantly affected. Glucose intolerance was apparent after iv glucose or arginine loads. Haloperidol and to a lesser extent phentolamine suppressed the cold-induced glucagon rise. Phentolamine and to a lesser extent haloperidol alleviated the cold-induced suppression of insulin release. Propranolol, naloxone, and atropine were relatively inactive. The cold-induced glucose intolerance was not corrected by phentolamine treatment. A marked resistance to iv insulin was apparent in these rats, which is in contrast to a normal sensitivity to iv glucagon.
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PMID:Glucagon and insulin secretion and their biological activities in hypothermic rats. 643 6


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