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

The study investigated the possible interrelationship between changes in sleep-wakefulness and body temperature, primarily induced by manipulation of the noradrenergic system in the medial preoptic area. Saline, norepinephrine, and its alpha- and beta-blockers were injected in the medial preoptic area and in some control areas of rats, during their sleeping and active periods. 5-Hydroxytryptamine was injected in the medial preoptic area in another group of animals. Simultaneous changes in sleep-wakefulness and the body temperature were continuously recorded. Norepinephrine produced hypothermia and arousal, whereas alpha-adrenergic blockers induced hyperthermia and sleep. These changes in body temperature and in sleep-wakefulness did not follow an identical time course. 5-Hydroxytryptamine induced hyperthermia without affecting sleep-wakefulness. It is suggested that there are different neuronal mechanisms in the medial preoptic area that bring about the drug-induced changes in temperature and sleep-wakefulness.
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PMID:Interrelationship of thermal and sleep-wakefulness changes elicited from the medial preoptic area in rats. 335 96

Concentrations of catecholamines in vitreous fluid and urine in guinea pigs dying of cold and the effects of freezing and autolysis on these parameters were studied. The analysis was performed by high performance liquid chromatography with electrochemical detection. Noradrenaline (NA) concentration in vitreous fluid was more than 20 times higher in the cold exposed animals than in controls (44.2 +/- 9.2 versus 2.0 +/- 1.0 ng/mL). Autolysis alone caused an increase to 33.5 +/- 7.7 ng/mL, and freezing alone to 13.4 +/- 5.3 ng/mL. The highest values were in the group with exposure, freezing, and autolysis. Adrenaline (A) concentration in the vitreous fluid increased fourfold (3.9 +/- 1.5 versus 0.7 +/- 0.5 ng/mL) in cold exposure and twofold as a result of autolysis. Dopamine (DA) concentration in vitreous fluid was elevated only in the group with exposure, freezing, and autolysis. The increase of NA concentration in urine was fivefold during the whole exposure (from 19.4 +/- 6.9 to 109 +/- 57.3 ng/mL), but A was increased by twentyfold (from 10 +/- 5.1 to 213.2 +/- 168.7 ng/mL), whereas DA concentration did not change. The increase of average excretion of NA to urine was eightfold during the first 6 h of exposure, and that of A tenfold. According to the present results, elevated concentrations of catecholamines in the vitreous fluid and urine can be used as a diagnostic aid for hypothermia death. Concerning the values of noradrenaline in the vitreous, the increase as a result of autolysis must be taken in account when interpreting the results.
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PMID:Catecholamines in the vitreous fluid and urine of guinea pigs dying of cold and the effect of postmortem freezing and autolysis. 378 3

Norepinephrine, serotonin, and bombesin administered intrahypothalamically affected thermoregulation in the deermouse, Peromyscus maniculatus. At a Ta of 22 degrees C, doses of 3 micrograms and 6 micrograms of NE resulted in transient hypothermia (maximum drop of 1.6 +/- 1.0 degrees C and 4.3 +/- 2.3 degrees C, respectively). A 1.5 microgram dose of 5-HT induced a persistent hyperthermia (maximum increase of 1.8 +/- 0.8 degrees C) which persisted for more than 2 h. A 6 microgram dose of 5-HT did not produce any significant effects. At a Ta of 22 degrees C, doses of 1 ng and 10 ng of bombesin produced a transient hyperthermia (maximum increase of 1.8 +/- 0.3 degree C and 2.1 +/- 1.2 degrees C, respectively) immediately postinjection. At a Ta of 5 degrees C, a 1 ng dose of bombesin resulted in a prolonged hypothermia (maximum decrease of 2.0 +/- 0.4 degrees C), while a 10 ng dose of bombesin produced a hyperthermic response (maximum increase of 1.3 +/- 0.8 degree C) at 2 h postinjection.
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PMID:Effects of intrahypothalamically administered norepinephrine, serotonin and bombesin on thermoregulation in the deermouse (Peromyscus maniculatus). 394 67

1 In unanaesthetized pigeons, kept at room temperature (20-23 degrees C) the effects on cloacal temperature were examined of catecholamines, phenoxybenzamine and propranolol, injected into the cerebral ventricles.2 Noradrenaline, adrenaline, dopamine and isoprenaline caused a fall in cloacal temperature.3 Phenoxybenzamine produced a long-lasting small rise in cloacal temperature. This rise is attributed to removal of the hypothermic effect of noradrenaline released continuously from adrenergic neurones ending in the anterior hypothalamus. Propranolol produced a slight fall in cloacal temperature.4 The hypothermic effects of noradrenaline, adrenaline and dopamine were prevented by phenoxybenzamine but not by propranolol. They are therefore attributed to activation of alpha-adrenoceptors.5 The hypothermic effect of isoprenaline was not prevented by either phenoxybenzamine or propranolol. The effect can therefore not be attributed to activation of either alpha or beta-adrenoceptors. Propranolol actually accentuated the isoprenaline-induced hypothermia.
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PMID:Effects of catecholamines on thermoregulation in pigeons. 445 63

1. Noradrenaline given directly into the lateral cerebral ventricles induced hypothermia in mice. This hypothermia was antagonized and eventually reversed to a hyperthermia by imipramine-like antidepressant drugs.2. The mechanism of action involved in this effect of antidepressant drugs has been studied using nortriptyline as a typical representative of antidepressant drugs.3. Nortriptyline pretreatment did not modify either the uptake, subcellular distribution, or the metabolism of (3)H-noradrenaline injected into the lateral cerebral ventricles.4. Nortriptyline had the same order of activity in reversing the hypothermia produced by the intraventricular injection of noradrenaline irrespective of whether it was given directly into the lateral cerebral ventricles or subcutaneously.5. Noradrenaline given subcutaneously caused hyperthermia in mice which antagonized and reversed the hypothermia induced by noradrenaline given directly into the lateral ventricles.6. The antagonism by both noradrenaline given subcutaneously and nortriptyline was reduced to the same degree by alpha- and beta-adrenoceptive receptor blocking agents.7. Nortriptyline, at dose levels required to antagonize and reverse the hypothermia induced by intraventricular injections of noradrenaline, potentiated the hyperthermia caused by noradrenaline given subcutaneously in conscious mice and the pressor responses to noradrenaline given either intravenously or into the lateral ventricles in anaesthetized mice.8. It is suggested that imipramine-like antidepressant drugs antagonize the hypothermia produced by intraventricular injections of noradrenaline by potentiating the hyperthermic effects of that part of the centrally administered noradrenaline that passes to the periphery rather than a direct central antagonism of the effects of noradrenaline.
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PMID:The reversal of the central effects of noradrenaline by antidepressant drugs in mice. 567 4

1. The hypothesis of Roberts & Broadley (1965) that noradnamine formation in the brain is responsible for endogenous depression has been investigated in mice.2. Injections of noradnamine given directly into the lateral ventricles caused convulsions and profound hypothermia, but were without effect if given subcutaneously.3. The hypothermia, but not the convulsions, induced by noradnamine was reversed by imipramine-like antidepressant drugs given before or after the injection of noradnamine. The convulsions but not the hypothermia were abolished by phenobarbitone.4. Increasing doses of nortriptyline produced a parallel shift of the hypothermic log dose-response curve for intraventricular injections of noradnamine to the right.5 The minimal effective dose of nortriptyline required to reverse noradnamine hypothermia was the same whether the nortriptyline was injected directly into the lateral ventricle or subcutaneously.6. No evidence was found to substantiate the claim that reserpine hypothermia is mediated by noradnamine formation in the brain.7. Intraventricular, but not intraperitoneal, injection of noradnamine caused a depletion of brain noradrenaline and an increase in brain 5-hydroxytryptamine. These changes did not result from the convulsive activity and were not modified by pretreatment with nortriptyline. No effect on heart noradrenaline levels was recorded.8. Noradrenaline, given subcutaneously, also antagonized the hypothermic response to noradnamine.9. The reversal of noradnamine hypothermia by both noradrenaline given subcutaneously and nortriptyline was blocked by alpha and beta-adrenoceptive receptor blocking agents.10. It is considered that the mode of action of the antagonism of noradnamine hypothermia by imipramine-like antidepressant drugs is a peripheral and not a central mechanism and probably results from a potentiation of the effects of circulating noradrenaline released by noradnamine.
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PMID:The interactions of noradnamine and imipramine-like antidepressant drugs. 576 31

1. Changes in temperature were determined following injection of noradrenaline, adrenaline, isoprenaline, dopamine and 5-hydroxytryptamine (5-HT) into the cerebral ventricles of the conscious mouse.2. Noradrenaline (1-20 mug) and dopamine (10-160 mug) caused falls in body temperature. Adrenaline (1-20 mug) caused a slight and transient rise in body temperature followed by a fall. Isoprenaline (5-20 mug) caused a rise in body temperature, hypothermia only occurring after very high doses (200 mug) of this catecholamine.3. alpha- and beta-adrenergic blocking agents, phentolamine (> 2 mug) and propranolol (> 5 mug) respectively, caused falls in body temperature when injected into the cerebral ventricles of the mouse.4. Specific drug antagonism studies were limited owing to the intrinsic effects of the alpha- and beta-adrenergic blocking agents. However, some evidence was obtained to indicate that noradrenaline mediated its effects through a central alpha-type adrenergic receptor.5. 5-HT (10-160 mug) caused a fall in body temperature. The action of this indoleamine and the catecholamines in regard to thermoregulatory function is discussed.
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PMID:Temperature changes produced by the injection of catecholamines and 5-hydroxytryptamine into the cerebral ventricles of the conscious mouse. 605 3

Noradrenaline (NA), adrenaline (ADR), isoprenaline (ISO) and dopamine (DA) were given through a chronically implanted cannula in the lateral cerebral ventricle of Mastomys natalensis. Low doses of NA (0.05-0.25 microgram) reduced rectal temperature while larger doses (0.35 microgram upwards) produced dose-dependent hyperthermia. The hypothermic effect was antagonised by alpha-adrenoceptor and the hyperthermia by beta-adrenoceptor antagonists. alpha-Methyl noradrenaline produced less hyperthermia but it antagonised the hyperthermic effect of NA. Adrenaline (0.1-10 microgram) was ineffective per se but when given after tolazoline it produced hyperthermia and after propranolol it produced hypothermia. The dose-dependent hyperthermia with isoprenaline (0.1-10 microgram) was blocked by propranolol and MJ-1999. Dopamine (0.5-20 microgram) and its agonists apomorphine, amantadine and BS 9641 produced hyperthermia which was antagonised by haloperidol and pimozide but not by alpha- or beta adrenoceptor antagonists. Noradrenaline (1.0 microgram) produced hypothermia at ambient temperature of 10 degrees C and 16 degrees C. It had no effect at 20 degrees C which seems to be the thermoneutral zone for mastomys. The hyperthermic effect at 33 degrees C was less than at 24 degrees C. Dopamine (10 micrograms) response was attenuated at 33 degrees C and unaffected at other ambient temperatures. It is concluded that alpha- and beta-adrenoceptors and DA-receptors exist in the central thermoregulatory mechanism in mastomys. The alpha-receptors are concerned with lowering the body temperature whereas the beta-receptors and DA-receptors are involved in raising it.
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PMID:The effect of intracerebroventricular administration of catecholamines and their antagonists on rectal temperature of Mastomys natalensis. 612 Apr 69

1. Norepinephrine (NE) and serotonin (5-HT) were simultaneously assessed in 4 discrete regions of the brain of the golden hamster. 2. Hypothalamic concentrations of both these amines are reported for the following groups: (1) normothermic controls; (2) heat acclimated; (3) cold acclimated; (4) helium-cold hypothermic; (5) rewarming; and (6) rewarmed. 3. Heat acclimated animals demonstrated approximately 35 and 25% decreases from control values for NE and 5-HT, respectively. Cold acclimated hamsters were not significantly different from controls. Helium-cold hypothermia resulted in approximately a 30 and 20% decrease in NE and 5-HT, respectively, with the latter returning to control values during rewarming. 4. The data provide indirect evidence for the involvement of NE in central pathways involving heat gain and 5-HT in pathways involving heat loss, and are discussed in terms of FELBERG & MYER'S (1964 J. Physiol., Lond. 173. 226-236) bioamine theory of thermoregulation.
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PMID:Brain norepinephrine and serotonin in the golden hamster during heat and cold acclimation and hypothermia. 612 3

Norepinephrine (NE), octopamine (OA) and phenethylamine (PEA) are easily destroyed by M.A.O. but we could show, even injected intraperitoneally that they are active upon tests used generally to reveal an "antidepressant" effect. This effect is especially studied by using antagonism of apomorphine, reserpine, oxotremorine-induced hypothermia. The psychopharmacological spectra of NE and OA are close to the one of salbutamol and the observed effects correspond to alpha- and beta-adrenergic stimulations. The PEA spectrum is similar to the one of amphetamine and the observed effects correspond to adrenergic stimulations and to a dopaminergic stimulation. The mechanisms involved in the tests realized to show an "antidepressant" effect could reflect an activity not only through endogeneous NA but also possibly through endogeneous OA and PEA.
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PMID:[Antidepressive effects of 3 endogenous monoamines: psychopharmacologic profiles of noradrenaline, octopamine and phenethylamine]. 642 65


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