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

Noradrenaline (5 microgram in 0.5 microliter) was microinjected into 87 different sites within the preoptic anterior hypothermic area of cat brain to determine the anatomical location most sensitive to the hypothermic action of the amine. At 26 of these sites noradrenaline produced a hypothermia greater than 0.5 degrees C. Such falls in body temperature were invariably accompanied by vasodilation and sometimes by a marked increase in respiratory rate. During the hypothermia most animals appeared sedated. Histological analysis of the sites where hypothermia was produced indicated that the site of maximum sensitivity occurred between the optic chiasm and the anterior commissure at A 15.0, L 2.5, H--2.5. The results are discussed in terms of the physiological control of body temperature.
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PMID:Precise location within the preoptic area where noradrenaline produces hypothermia. 69 73

Plasma concentrations of adrenaline, noradrenaline, and free fatty acids were measured at different stages of cardiac operations in which hypothermia and bypass were used. The rise of adrenaline, noradrenaline, and free fatty acid concentrations in plasma is consistent with the concept that these are important compounds in stress situations such as hypothermia and surgical operations. There is a more marked release of adrenaline and it may be a more specific hormone in response to hypothermia and bypass than is noradrenaline in man.
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PMID:Catecholamines and free fatty acids in plasma of patients undergoing cardiac operations with hypothermia and bypass. 71 3

1 Noradrenaline (0.2 to 20 micrograms) and carbachol (0.1 to 1 microgram) injected into the preoptic/anterior hypothalamic area, evoked dose-dependent falls in core temperature at all sites tested, followed in most experiments by delayed increases that were not dose-related. Muscarine (0.1 to 10 microgram) produced effects similar to those evoked by carbachol. 2 These falls in core temperature were associated with increases in tail temperature, locomotor activity and CO2 elimination (a measure of metabolic rate). 3 The temperature responses to noradrenaline (10 microgram) and to carbachol (1 microgram) were antagonized by intrahypothalamic injections of phentolamine (10 microgram) and atropine (1 microgram), respectively. 4 Analysis of the temperature responses and their respective latencies indicates that carbachol-induced hypothermia was mediated by cholinoceptors in the anterior hypothalamus, whereas hypothermia after noradrenaline was mediated by adrenoceptors throughout the preoptic/anterior hypothalamic area. 5 Vasodilatation of the tail blood vessels contributed significantly to the hypothermia evoked by carbachol, and to that evoked by injections of noradrenaline into the anterior hypothalamus. 6 Hypothermia induced by noradrenaline injection into the preoptic area, was mediated by effector mechanisms additional to non-evaporative heat loss.
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PMID:Effects of noradrenaline and carbachol on temperature regulation of rats. 76 Aug 90

The action of endotoxin, trypsin or hypothermia on the vascular reactivity to catecholamines was investigated in rabbits, and with trypsin in normothermic dogs as well. In rabbits, LD10 of Escherichia coli 0111 endotoxin increased the blood pressor effect of i.v. adrenaline or noradrenaline with maxima at 60-90 min. LD50 endotoxin elicited a vascular hyporeactivity to catecholamines within an hour. 22 hours later, however, a hyperreactivity to catecholamines developed. At this time, repeated administration of LD50 endotoxin did not reduce the increased catecholamine responsiveness. Trypsin (i.v. 1.5 mg/kg) also potentiated the pressor effect of catecholamines in rabbits and dogs with maxima at 5-10 min. Higher trypsin doses induced a hyporeactivity. LD50 endotoxin in a single or a repeated dose after 22 hours did not decrease the blood pressure of cooled rabbits and failed to alter the vascular reactivity to adrenaline or noradrenaline. The blood pressure effect of trypsin differed in character in normo- and hypothermic rabbits, depending on the depth of cooling. Low body temperature eliminated the potentiating effect of trypsin to the blood pressor action of catecholamines. In normothermic rabbits pretreated with amino-pyrine and phenylbutazone, the blood pressure and the catecholamine potentiation effects of endotoxin or trypsin were inhibited or considerably reduced. The results support the significance of altered vascular reactivity to catecholamines under different pathologic conditions where endotoxin and/or proteases may occur.
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PMID:Effect of endotoxin and trypsin on the blood pressor response to catecholamines in normo- and hypothermic rabbits. 78 25

1 The hypothermia produced by intraventricular injections of thyrotropin releasing hormone (TRH) in unanaesthetized cats has been investigated. 2 TRH is more potent than either noradrenaline or calcium ions. It is estimated that the equi-potent molar ratio for TRH: noradrenaline:calcium is 1:900:27,000. 3 TRH injections is also produce profuse salivation, tachypnoea, cutaneous vasodilatation and frequently defaecation and vomiting. It is considered that the increased respiration is a major cause of the hypothermia. 4 Prior administration of phentolamine antagonized noradrenaline-induced hypothermia but did not affect hypothermia produced by TRH or calcium ions. Pretreatment with alpha-methyltyrosine did not affect the hypothermia induced by TRH, calcium ions or noradrenaline. 5 The calcium antagonists verapamil and xylocaine did not antagonize hypothermia induced by an injection of calcium ions. 6 The constituent amino acids of TRH did not produce hypothermia either individually or collectively. Thyroxine sodium produced a rise in temperature that was slow in onset, consistent with its known metabolic effects. TSH produced a small hypothermia unrelated to dose.
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PMID:A comparison between the hypothermia induced by intra-ventricular injections of thyrotropin releasing hormone, noradrenaline or calcium ions in unanaesthetized cats. 82 97

Role of brain monoamines in the hyprothermic activity of cannabis resin (CI) in albino rats was studied using agents which influence monoamine synthesis, storage, release, reuptake, metabolism and receptor activity and monoaminergic neuronal activity. Delta-9-tetrahydrocannabinol content of resin was estimated to be 17%. Reserpine was used for comparison. CI was given orally in the dose of 50 mg/kg. Nialamide (NM) and alpha-methyl-metatyrosine (MMT) caused slight hyperthermia. p-Chlorophenylalanine (PCPA), alpha-methol-p-tyrosine (MPT), 5,6-dihydroxytryptamine (DHT, icv) and 6-hydroxydopamine (6-HD, icv) had no effect on body temperature. alpha-Methyl-dopa (m-Dopa), diethyldithiocarbamate (DDC), DDC with l-Dopa, gammabutyrolactone (GBL), phentolamine (PHENT), phenoxybenzamine (PBZ), propranolol (PROP) and imipramine (IMP) produced hypothermia. Hyprothermic activity of CI was potentiated by NM and PCPA, unaffected by DHT and m-Dopa, blocked by MMT, MPT, 6-HD, GBL, PHENT, PROP and chlorpromazine (CPZ), inhibited by DDC, DDC and l-Dopa and PBZ. CI induced hyperthermia in tolerant rats could be reversed to hypothermia by IMP. Reserpine hypothermia was blocked by NM, MPT, 6-HD and CPZ. There was a partial cross tolerance between cannabis and reserpine. Studies indicate that the hypothermic activity of CI similar to that of reserpine is mediated through central catecholamines and not 5-HT, and that noradrenaline is involved and not dopamine. However, the mechanism of action of cannabis and reserpine on noradrenergic neurone seems to be different.
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PMID:Role of catecholamines in the hypothermic activity of cannabis in albino rats. 82 62

In rats housed normally (aggregated, food and water ad lib) for fourteen days delta8-tetrahydrocannabinol (THC) produced mild sedation and minimal hypothermia. An increase in noradrenaline synthesis was observed, but brain dopamine metabolism was unchanged. In rats removed from this 'normal' environment to conditions of isolation and food deprivation for 24 h THC produced immobility, marked hyper-reactivity, and hypothermia. Brain noradrenaline metabolism was unchanged by THC under these conditions, but significant changes in striatal dopamine metabolism were observed. These changes are consistent with increased dopamine reuptake in striatum produced by this combination of THC and novel environment. It is suggested that some of the behavioural effects of cannabis administered under stressful conditions may be related to alterations in striatal dopamine metabolism.
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PMID:Environmental stress as a factor in the response of rat brain catecholamine metabolism to delta8-tetrahydrocannabinol. 83 73

5-hydroxydopamine, unspecific centrally acting false neurotransmitter. Acta Physiol. Pol., 1977, 28 (1): 13-22. 3,4,5-trihydroxyphenetylamine-5-hydroxydopamine (5-OHDA) injected intracerebro-ventricularly decreases the level of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in different parts of the rat brain. It does not affect acetylcholine level. 5-OHDA causes dose-dependent hypothermia, transient hypertension and depression of locomotor and exploratory activity in rats. This behavioral phenomena are reversed by central chemical sympathectomy elicited by 6-hydroxydopamine. It is concluded that 5-OHDA is an unspecific centrally acting false transmitter.
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PMID:5-hydroxydopamine, unspecific centrally acting false neurotransmitter. 86 21

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

The effects of viloxazine, a clinically effective antidepressant, on noradrenaline (NA) and 5-hydroxytryptamine (5-HT) uptake and various related pharmacological activities were determined and compared to those of the tricyclic antidepressants desimipramine, imipramine, and amitriptyline. Viloxazine inhibitied [3H]NA uptake in the mouse and rat heart, being maximally about one half as potent as imipramine with a similar onset, but shorter duration of action than imipramine. The drug did not inhibit [3H]NA uptake in rat medulla or hypothalamus in contrast to desimipramine and imipramine, but it did alter [3H]NA metabolites in a similar manner. Viloxazine, like desimipramine, was a weak blocker of mouse brain 5-HT uptake, but differed from desimipramine as it poteniated 5-HT-mediated functions in the mouse and rat, as did imipramine and amitriptyline, the latter drugs being relatively potent blockers of 5-HT uptake. Viloxazine potentiated the L-DOPA behavioural syndrome in the mouse, antagonized reserpine-induced ptosis and hypothermia in the mouse, and inhibited gastric acid secretion in the rat, but was less potent than the tricyclic antidepressants. No appreciable in vivo inhibition of monoamine oxidase (EC 1.4.3.4.) activity in the mouse was exhibited. Like imipramine, the drug potentiated the ocular effects of L-adrenaline in the rabbit. It was similar to imipramine in potency in potentiating the apomorphine-induced gnawing in the mouse. The drug antagonized oxotremorine-induced hypothermia in the mouse but differed from the tricyclic antidepressants in not exhibiting the anticholinergic effects of blocking the tremors, salivation and lacrimation. Thus, viloxazine exhibits activities related to the biogenic amines both similar to and different from the tricyclics desimipramine, imipramine, and amitriptyline. These actions appear to be of relevance with respect to the antidepressant action of this drug.
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PMID:Effects of viloxazine, an antidepressant agent, on biogenic amine uptake mechanisms and related activities. 97 78


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