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

1 The cerebral ventricles of dogs under intravenous pentobarbitone sodium anaesthesia, were perfused with artificial cerebro-spinal fluid (CSF) at a rate of 0.4-0.5 ml/min from the ventricular to the aqueductal cannulae. The effluent was collected from the aqueductal cannula in 20 min samples. The animals' temperatures were recorded from the rectum.2 gamma-Aminobutyric acid (GABA) 0.1-5 mg when injected into the ventricles produced variable temperature effects. Doses of 0.1 and 0.5 mg always produced hyperthermia and 1 and 5 mg doses sometimes produced hyperthermia and sometimes hypothermia.3 Intraventricular perfusion with 2-bromolysergic acid diethylamide (BOL) and hyoscine did not block hyperthermia. Tests on the rat isolated stomach strip or the guinea-pig isolated superfused ileum for the possible release, respectively, of 5-hydroxytryptamine or acetylcholine by GABA were negative.4 When tested for the presence of prostaglandin E(PGE)-like substances on the isolated rat stomach strip, both the control effluent and the GABA effluent showed activity, the latter being much more potent. There was a temporal correlation between this effect and hyperthermia. Intraventricularly administered sodium salicylate converted the GABA-induced hyperthermia to hypothermia and blocked the release of PGE-like substances.5 Hypothermia induced by GABA alone or in the presence of sodium salicylate was associated with the release of noradrenaline into the effluent.6 Intraventricular administration of GABA in reserpinized dogs produced hyperthermia and not hypothermia. Similar results were obtained with phentolamine perfusion in normal dogs.7 Perfusion with calcium-free solution blocked both the noradrenaline-releasing and hypothermic actions of GABA.8 It is concluded that hyperthermia associated with intraventricular injections of GABA is due to the release of PGE-like substance and hypothermia is due to the release of noradrenaline.
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PMID:Analysis of the effects on body temperature of intracerebroventricular injection in anaesthetized dogs of gamma-aminobutyric acid. 415 52

1. Intraperitoneal administration of graded doses of tetrahydronaphthylamine (THN) to rats caused a dose dependent decrease in body temperature.2. Intracisternal injection of graded doses of THN induced hypothermia, and implantation of crystalline THN rostral to the medial preoptic area and caudal to the striatum, caused hyperthermia.3. Pretreatment of the rats with a MAO inhibitor changed the hypothermia into hyperthermia.4. Intraperitoneal injection of 5-hydroxytryptophan caused a hypothermia which could be reversed into hyperthermia when the rats were pretreated with a MAO inhibitor.5. Pretreatment with parachlorophenylalanine enhanced the THN-induced hypothermia.6. Depletion of brain monoamines by Ro-4-1284 in combination with an inhibition of the biosynthesis of noradrenaline (diethyldithiocarbamate) changed the THN-induced hypothermia into hyperthermia.7. It is concluded that THN affects body temperature in rats by two central mechanisms, viz. a decrease mediated by noradrenaline, probably in the hypothalamus, and an increase which might be mediated by 5-hydroxytryptamine rostral to the medial preoptic area.
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PMID:Role of noradrenaline and 5-hydroxytryptamine in tetrahydronaphthylamine-induced temperature changes in the rat. 425 29

1. Intraperitoneal injection of graded doses of ketamine produced a dose-dependent fall in body temperature of rats. Similarly, intracerebral injection of much smaller doses produced hypothermia.2. Pretreatment of the rats with p-chlorophenylalanine (PCPA) greatly attenuated the hypothermic response to ketamine whereas the intraperitoneal injection of 5-hydroxytryptophan in PCPA-treated rats restored the hypothermic effect of ketamine.3. Depletion of the brain monoamines by reserpine completely prevented the ketamine-induced hypothermia. Treatment with sodium diethyldithiocarbamate (DEDTC), however, did not modify the hypothermic effect of ketamine.4. Pretreatment of the rats with pargyline potentiated the ketamine-induced hypothermia.5. Depletion of brain monoamines by reserpine in combination with inhibition of noradrenaline biosynthesis (DEDTC) resulted in a long lasting fall in temperature which was not modified by ketamine.6. When the ambient temperature was raised from 26 degrees C to 32 degrees C, ketamine-induced hypothermia was much reduced and superimposed on a hyperthermia which occurred in all animals.7. It is concluded that ketamine produces hypothermia in rats possibly through the release of 5-hydroxytryptamine in the hypothalamus and that this effect is similar in some respects to that produced by morphine in non-tolerant rats.
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PMID:Role of 5-hydroxytryptamine in ketamine-induced hypothermia in the rat. 427 91

1. Ouabain given by intracerebroventricular injection to mice in small doses (0.1-0.4 mug) produced a dose related depression of central nervous activity, characterized by a reduction in spontaneous locomotor activity, hypothermia, catalepsy and ptosis, lowered body posture and lack of response to external stimuli. Doses above 0.4 mug were excitatory, convulsant and lethal.2. The depressant effects could be antagonized by (+)-amphetamine, desmethylimipramine, dibutyryl cyclic 3'5'-adenosine monophosphate and caffeine.3. The MAO inhibitor nialamide produced only a small antagonism of ouabain, resulting in a greater rate of recovery from the depressant effects of ouabain.4. The depressant effects were associated with a marked elevation of whole-brain dopamine levels with little change in noradrenaline or 5-hydroxytryptamine.5. The dopamine-beta-hydroxylase inhibitor sodium diethyldithiocarbamate, administered by intracerebroventricular injection, produced effects qualitatively similar to those seen after ouabain.6. An interference with central transmitter function is postulated as a possible mode of action of intracerebroventricularly injected ouabain.
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PMID:Pharmacological properties of centrally administered ouabain and their modification by other drugs. 432 23

1. In cats, the effects of tranylcypromine and pheniprazine, two monoamine oxidase (MAO) inhibitors with strong amphetamine-like actions, of pargyline, an inhibitor without amphetamine-like actions, and of amphetamine itself, were examined on the hypothermia produced by a 2 hr period of halothane inhalation.2. The hypothermia was prevented by intraperitoneal injections of the three MAO inhibitors. Tranylcypromine and pheniprazine acted in doses of a few milligrams, pargyline in doses of over 100 mg.3. The hypothermia was prevented by injections into the cerebral ventricles of tranylcypromine and pheniprazine, in doses which were effective also on intraperitoneal injection; intraperitoneal injections were sometimes more effective. The large doses of pargyline needed to prevent the hypothermia when injected intraperitoneally were not tested by the intraventricular route, as the injections had to be made in a volume of 0.1 ml. In smaller doses intraventricular pargyline was not effective.4. The hypothermia was prevented by an intraperitoneal or intraventricular injection of amphetamine in a dose as little as 1 mg; intraperitoneal injections were sometimes more effective.5. The effects of tranylcypromine and pargyline given intraperitoneally, and of amphetamine given intraventricularly as well, were also examined on the hypothermia produced by an intraventricular injection of 200 mug noradrenaline. The two MAO inhibitors and amphetamine prevented the hypothermia, or greatly reduced it.6. It is concluded (a) that even on intraventricular injection the MAO inhibitors must first be absorbed into the blood stream before they can prevent the hypothermia of a halothane anaesthesia; (b) that their action may not be solely on the anterior hypothalamus; and (c) that they may not act only through MAO inhibition.
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PMID:Effects of monoamine oxidase inhibitors and amphetamine on hypothermia produced by halothane. 439 31

1. The effect on rectal temperature of adrenoceptor blocking agents, injected through a cannula chronically implanted into a lateral cerebral ventricle, was examined in unanaesthetized rabbits, cats and rats, kept at room temperature (19-22 degrees C).2. In rabbits, the alpha-adrenoceptor blocking agent phenoxybenzamine (50 or 100 mug) produced marked hypothermia when injected intraventricularly but not when injected intravenously. In some rabbits as little as 1 mug was effective on intraventricular injection. Phentolamine and ergotamine, the other alpha-adrenoceptor blocking agents examined, had a much weaker hypothermic action when injected intraventricularly, whereas the beta-adrenoceptor blocking agents propranolol, pronethalol and Trasicor had no effect.3. In rabbits in which the noradrenaline stores of the hypothalamus were depleted by intraventricular injections of reserpine, the hypothermic effect of phenoxybenzamine was abolished and remained abolished for a few days.4. In cats, an intraventricular injection of phenoxybenzamine (200 mug) produced long-lasting hyperthermia, but not in all cats, and only with the first, or the first two or three injections. Injected intraperitoneally, this dose had no effect on temperature. Phentolamine (100 or 200 mug) had a very weak hyperthermic effect and phentolamine (500 mug), a hypothermic effect, but only on intraventricular injection, whereas ergotamine (100 and 200 mug) had a weak hyperthermic effect both on intraventricular and intraperitoneal injection. Propranolol and Trasicor had no effect on temperature when injected intraventricularly.5. In rats, phenoxybenzamine (5 or 20 mug) produced long-lasting hypothermia on intraventricular injection.6. Some of the temperature effects produced by intraventricular injections of the alpha-adrenoceptor blocking agents are explained on the assumption that they prevent the effect on temperature produced by a continuous release of noradrenaline from adrenergic neurones innervating the anterior hypothalamus.
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PMID:Effects of adrenoceptor blocking agents on body temperature. 440 May 28

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. An intravenous injection into rats of 1 mg/kg (-)-Delta(9)-tetrahydrocannabinol Delta(9)-THC) had no effect on rectal temperature and produced in the subcellular fractions of the brain a shift of 5-hydroxytryptamine (5-HT) from the particulate or ;bound' 5-HT to the supernatant or ;free' fraction, whereas the noradrenaline (NA) decreased in both fractions.2. Pretreatment of rats by an intravenous injection of 1 mg/kg Delta(9)-THC three times a week for four weeks, prevented the hypothermia and the reduction in brain 5-HT produced by an intraperitoneal injection of 15 mg/kg reserpine given 24 h after the last Delta(9)-THC injection.3. Pretreatment of rats by a single intravenous injection of 1 mg/kg Delta(9)-THC prevented the hypothermia and reduction in brain 5-HT produced by an intraperitoneal injection of reserpine given 1 h before. The reduction in brain NA was not prevented except at the 18 h time interval.4. An injection of 1 mg/kg Delta(9)-THC intravenously into rats 3 h after an intraperitoneal injection of reserpine accentuated the reserpine hypothermia as well as the reduction of 5-HT but not of NA in the brain.5. The reserpine hypothermia was not prevented by a single intravenous injection of 1 mg/kg Delta(9)-THC when cinanserin, a 5-HT inhibitor, was injected 30 min before the reserpine.
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PMID:The effects of (-)-delta9-tetrahydrocannabinol on reserpine-induced hypothermia in rats. 479 31

1. Chlorpromazine 15 mg/kg, given daily to cats for 2 weeks, produced a rise in homovanillic acid (HVA) content of the caudate nucleus, whereas the same dose of thioridazine lacked this effect. Of these two drugs, only chlorpromazine causes a high incidence of drug-induced Parkinsonism in man.2. In the mouse, chlorpromazine, thioridazine and haloperidol increased striatal concentrations of HVA and accelerated the disappearance of dopamine (DA) after inhibition of catecholamine synthesis with alpha-methyltyrosine. Low doses of the three compounds increased, whereas high doses reduced, the concentration of DA in the striatum. In their effects on the DA metabolism of the mouse, chlorpromazine and thioridazine had the same potency, but haloperidol was between 10 and 100 times more active than the other two drugs. In producing hypothermia and sedation, the three compounds were equiactive.3. Oxypertine, another drug apt to produce Parkinsonism in man, caused a severe reduction in striatal DA and hypothalamic noradrenaline (NA). Though the clinical signs produced in the mouse were indistinguishable from those seen after the same dose of chlorpromazine, the biochemical changes in the brain were thus quite different.4. Though all the drugs used caused temporary motor disabilities in animals, these bore no resemblance to human Parkinsonism, even when treatment was continued for 7 weeks or more as it was in cats and monkeys. The latter were treated with chlorpromazine 7.5 mg/kg daily, a dose chosen to avoid loss of weight and which may have been too small to produce toxic side-effects. It caused no changes in striatal DA turnover.5. Even at the high dose of 50 mg/kg, phenoxybenzamine did not increase DA turnover in mouse brain, but it sedated the mice as did the tranquillizers.6. Atropine sulphate, 25 mg/kg, reduced the HVA content of mouse striatum and partially antagonized the rise in HVA produced by phenothiazines. The effect was surmountable. Possible modes of action of atropine are discussed.7. At present we know of two types of biochemical changes which may occur in the brain of animals after treatment with drugs apt to cause Parkinsonism in man: a loss of cerebral catecholamines, as seen after reserpine or oxypertine, or an increase in turnover of DA as after phenothiazines and butyrophenones.
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PMID:Effect of drugs used in psychoses on cerebral dopamine metabolism. 498 1

1. The cerebral ventricles of the unanaesthetized monkey were perfused at a rate of 50-100 mul./min with artificial cerebrospinal fluid (c.s.f.) containing 11.0-34.0 mM excess sodium or 23.9-47.9 mM excess calcium ions. By repeated perfusions, a marked hyperthermia elicited by excess sodium or deep hypothermia by excess calcium was sustained for up to half a day.2. During the sodium-induced hyperthermia or calcium-induced hypothermia, the monkey thermoregulated adequately around the new level of temperature in response to either 50 or 150 ml. water heated to 58 degrees C or chilled to 0 degrees C and given by the intragastric route. Cold water produced a transient hypothermia after which temperature returned to the pre-load level; hot water given in the same way evoked a short-lasting hyperthermia, and again the temperature returned just to the new setpoint level.3. Perfusions at 50 mul./min of isolated areas of the diencephalon by means of push-pull cannulae with a solution containing 11.0-34.0 mM excess sodium ions or 11.3-47.9 mM excess calcium ions altered the body temperature of the monkey only when the sites of perfusion were located in the mammillary region of the posterior hypothalamus. Following the prolonged hyperthermia produced by excess sodium ions or the deep hypothermia evoked by excess calcium ions in the push-pull perfusion fluid, the monkey thermoregulated around the new temperature level again in response to 150 ml. of either hot or cold water given in the stomach.4. Chelation of calcium ions within the ventricles by perfusing EGTA through the cerebral ventricles caused a long-lasting elevation in temperature. When EGTA was perfused directly in the posterior hypothalamus by means of push-pull cannulae, a profound hyper-pyrexia ensued which could be abolished immediately by perfusing a solution of excess calcium at the same diencephalic site.5. During the calcium-induced hypothermia, the heart rate declined but the electrical activity of the cortex was relatively unchanged. Feeding was also elicited in the hypothermic monkey by noradrenaline microinjected at a site in the hypothalamus at which eating was evoked when the body temperature was normal.6. The evidence supports the hypothesis that in the primate, the inborn mechanism which establishes the set-point for body temperature at 37 degrees C is the constancy in the intrinsic ratio between sodium and calcium ions within the posterior hypothalamus. If the set-point is elevated or lowered by a disturbance of the balance between these two cations, the monkey nevertheless can thermoregulate normally around the new level of body temperature.
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PMID:Thermoregulation around a new set-point' established in the monkey by altering the ratio of sodium to calcium ions within the hypothalamus. 500 28


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