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

The pharmacological activities of amineptine (S 1694) and (+)-amphetamine and their interaction with biogenic amines have been examined in rats. The locomotor activity, stereotyped behaviour and hypothermia induced by amineptine were similar to but not as marked as those produced by (+)-amphetamine, and there was little or no anorectic action. Amineptine does not modify the concentrations of brain noradrenaline or acetylcholine which are respectively reduced and increased by (+)-amphetamine. Moreover, amineptine does not affect significantly the decrease of brain noradrenaline induced by an intraventricular injection of 6-hydroxydopamine, an effect significantly antagonized by (+)-amphetamine. On the other hand, like amphetamine, amineptine significantly reduces the effect of 6-hydroxy-dopamine on brain dopamine. Both drugs increase the striatal concentrations of homovanillic acid and show a cross tolerance in this action. Therefore they could act similarly on the striatal dopaminergine system. Amineptine thus appears to be a new type of antidepressant with a brain biochemical profile differing from that of other drugs used in depressive disorders.
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PMID:Biochemical and pharmacological studies on amineptine (S 1694) and (+)-amphetamine in the rat. 2 Dec 61

Cocaine injected intraperitoneally into rats resulted in a dose-dependent hypothermia. Intracerebral injection of smaller doses also produced a fall in body temperature. In rabbits and guinea-pigs, cocaine produced hyperthermia, in mice and chicks it produced hypothermia while inconsistent changes were produced in goats. Pre-treatment of rats with 6-hydroxydopamine, alpha-methyl-m-tyrosine or haloperidol significantly antagonized the cocaine hypothermia. Pre-treatment of the rats with either hyoscine or methscopolamine resulted in some but non-significant attenuation of the cocaineinduced hypothermia. Pre-treatment with p-chlorophenylalanine, however, did not modify the cocaine hypothermia. Pargyline pre-treatment significantly antagonized the hypothermic action of cocaine. It is suggested that cocaine may cause the release of noradrenaline centrally or it may potentiate its action by interfering with the uptake mechanism. It is also possible that cocaine may have a direct effect on the heat regulating centre in the hypothalamus.
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PMID:Hypothermic effect of cocaine in rats. 13 13

The results of our recent investigations have suggested that tolerance and cross-tolerance development to motor-impairing and hypothermic effects of ethanol was slowed when brain serotonin (5-HT) was extensively depleted by treatment with p-chlorophenylalanine (p-CPA). These findings have been extended by the observation that p-PCA also slowed the development of tolerance to motor-impairing effects of barbital whether tolerance was tested repeatedly in the same animal or in separate subgroups being tested only once. Additional support was provided by the demonstration that intracerebral injection of 5,7-dihydroxytryptamine (-DHT), which is known to deplete 5-HT markedly, also slowed the development of tolerance to motor-impairing and hypothermic effects of ethanol. In addition, when brain 5-HT level was elevated by administration of L-tryptophan, the rate of tolerance development to ethanol, as measured by motor impairment and hypothermia, was accelerated. In contrast to 5,7-DHT, intracerebral injection of 5,6-DHT was surprisingly found to accelerate the development of tolerance to ethanol. Upon further investigation, however, it was determined that the 5,6-DHT treatment depleted brain 5-HT levels by only 20% and, in addition, resulted in the development of supersensitivity. These results further confirm and extend the generality of our observations that 5-HT may be involved in the development of tolerance and cross-tolerance to sedatives. The possibility of a non-specific vs. specific effect of the serotoninergic system (as well as other aminergic systems) in tolerance and neuroplasticity deserves further investigation. The possible significance of these findings and the role of 5-HT (and noradrenaline) in the mechanism of tolerance are discussed in terms of analogy to enzyme or receptor mechanism.
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PMID:Role of serotonin in tolerance to ethanol and barbiturates: evidence for a specific vs. non-specific concept of tolerance. 16 Aug 66

In 5--10 day-old kittens at thermoneutral environmental temperature cerebroventricular injections of 10 microgram serotonin or noradrenaline caused hyperthermia and hypothermia, respectively. Central injections of 20 and 200 ng prostaglandin E1 induced hyperthermia. Monophasic fever followed the cerebroventricular injections of 0.2 or 0.002 microgram E. coli endotoxin, both in thermoneutral and moderately cool environments. In kittens pretreated with para-chlorophenylalanine (PCPA) the endotoxin induced rise in body temperature was attenuated within 60 to 90 min after the endotoxin. Indomethacin pretreatment prevented the first part of the febrile response and only a slight temperature rise occurred after a long latency. Central injections of phentolamine did not modify the fever response, while centrally applied propranolol modified the fever course so that it resembled that seen in PCPA treated kittens. The central mediation of endotoxin fever in the kitten is complex, despite that the pattern of the temperature change is simple (monophasic). Arachidonic acid metabolites and serotonin of the central nervous system may be involved in the reaction, while the activation of central noradrenergic mechanisms does not seem to be indispensable for the response. The changes in mediators are similar to those in newborn guinea pigs, although the fever course is different in the two species.
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PMID:Endotoxin fever in the newborn kitten. The role of prostaglandins and monoamines. 16 15

1. Adenosine 3',5'-monophosphate (cAMP), its dibutyryl derivative (Db-cAMP) and other adenine nucleotides have been micro-injected into the hypothalamic region of the unanaesthetized cat and the effects on body temperature, and on behavioural and autonomic thermoregulatory activities observed. 2. Db-cAMP and cAMP both produced hypothermia when applied to the pre-optic anterior hypothalamus. With Db-cAMP the hypothermia was shown to be dose dependent between 50 and 500 mug (0-096-0-96 mumole). 3. AMP, ADP and ATP also produced hypothermia when injected into the pre-optic anterior hypothalamus. 4. The order of relative potencies of the adenine nucleotides with respect both to the hypothermia produced and to the autonomic thermoregulatory effects observed were similar. Db-cAMP was most potent and cAMP least. 5. Micro-injection into the pre-optic anterior hypothalamus of many substances including saline produced in most cats a non-specific rise in body temperature apparently the result of tissue damage. Intraperitoneal injection of 4-acetamidophenol (paracetamol 50 mg/kg) reduced or abolished this febrile response. 6. The hypothermic effect of the adenine nucleotides has been compared with the effects produced in these same cats by micro-injections of noradrenaline, 5-hydroxytryptamine, a mixture of acetylcholine and physostigmine (1:1), EDTA and excess Ca2+ ions. 7. It is concluded that as Db-cAMP and cAMP both produce hypothermia, it is unlikely that endogenous cAMP in the pre-optic anterior hypothalamus mediates the hyperthermic responses to pyrogens and prostaglandins.
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PMID:The effects of cyclic adenosine 3',5'-monophosphate and other adenine nucleotides on body temperature. 17 Mar 96

The content of the free fatty acids, ketone bodies, total glycogen, glucose, adrenaline and noradrenaline and morpho-histochemical picture of the tissues of neuro-endocrinal system (hypophysis and adrenal) in the brain, heart, liver, skeletal muscles and blood of the white non-linear rats, were studied 2-3 min adaptation to complex atmosphere changes: gradual increase of the CO2, decrease of the O2, and cooling (in the condition of deep hypothermia the rectal temperature was--RT--19.1 +/- 0.1 degrees C). The same parameters were studied in 48 hrs after the same training (at normothermia) and in 2-3 min. after the same repeated training in 48 hrs after the first one, at RT--20.2 +/- 0.1 degrees C. The fluctuating character of the metabolism and of the regulating systems was shown.
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PMID:[Character of metabolism and regulating role of cholinoreactive tissue systems during hypercapnia, hypoxia and cooling]. 19 72

1. Previous work from our laboratory has shown that cannabis induces aggressive behaviour in rats that have been deprived of rapid eye movement (REM) sleep. It was suggested that this effect was related to brain catecholamines, with dopamine playing an agonist role and noradrenaline an inhibitory one. The present paper describes new experiments dealing with this subject. 2. Previous REM sleep-deprivation enhanced both delta9-tetrahydrocannabinol (THC)-induced hypothermia and nomifensine effects on aggressive behaviour. 3. A marihuana extract decreased brain dopamine turnover in REM sleep-deprived rats, an effect not observed in non-deprived rats. Noradrenaline metabolism was not altered. 4. Fighting behaviour was elicited in REM sleep-deprived rats treated with 4 different dopamine-beta-hydroxylase inhibitors. 5. Apomorphine, nomifensine and delta9-THC administered to non-deprived rats pretreated with bis(4-methyl-1-homopiperanzinyl-thiocarbonyl) disulphide (Fla-63), induced fighting behaviour. 6. Nomifensine and apomorphine induced fighting in non-deprived rats pretreated with delta9-THC. 7. Clonidine inhibited the fighting elicited in REM sleep-deprived rats by either delta9-THC or Fla-63 pretreatment. 8. The data are discussed in terms of the influence of REM sleep-deprivation (or the stress associated with deprivation) on the response to dopaminergic drugs and cannabis. Taken together they emphasize the participation of brain dopamine and noradrenaline systems in the aggressive behaviour studied.
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PMID:Cannabis, catecholamines, rapid eye movement sleep and aggressive behaviour. 20 20

A short review of the role of cyclic nucleotides and prostaglandins (PGs) in normal and pathological functions of the heart is given. Possible interrelationships of these two regulatory systems have been studied by using spontaneously beating rat atria preparations. Addition of noradrenaline (NA) to the incubate (1 . 10(-6) M) caused an increase in amplitude and frequency which was preceded and parallelled by an elevation of the tissue cAMP level. A transient increase in cGMP and PGE values was also seen. Propranolol (5 . 10(-6) M) abolished the increase in amplitude and frequency as well as in cAMP and PGE concentrations. Indomethacin (1 . 10(-5) M) inhibited the formation of PGE. The increase in cGMP was blocked by phenoxybenzamine. Interchange between beta- and alpha-receptors according as the temperature is lowered has been described earlier. Hypothermia (20 degrees C) had a positive inotropic effect on the atria and increased the tissue cAMP concentration. Loading of the atria caused an increase in cAMP without any effects on cGMP or PGs. Slight hypoxia did not change the cAMP or PG levels, but elevated the cGMP values. Arrhythmias induced by hypo- or hyperpotassemia did not modify the biochemical parameters measured. PGF2alpha (1. 10(-5) M) normalized the atrial rhythm and increased the amplitude without changing cyclic nucleotide or PG levels. PGE1 (1 . 10(-4) M) increased the amplitude of normorhythmic atria and the tissue concentration of cAMP. PGE2 was the only PG tested which stimulated the heart adenylate cyclase in vitro. There seems to be close but complicated relationships between cyclic nucleotides and PGs in the heart.
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PMID:The role of cyclic nucleotides and prostaglandins in heart function. 21 11

1 The effect of intrahypothalamic phentolamine (1 and 1 microliter of a 10 microgram/microliter solution) on hypothermia induced by intramuscular injection of noradrenaline (NA, 2 mg/kg) at different times (2, 10, 20 min) after phentolamine was investigated in pigeons. 2 Administration of phentolamine shortly before NA was shown to attenuate hypothermic responses to NA. 3 It is suggested that the attenuation is due to blockade of central hypothermic effects of intramuscular NA. 4 The mapping of injection sites in the brains was carried out.
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PMID:Effect of intrahypothalamic phentolamine on hypothermia produced by peripheral noradrenaline in the pigeon. 33 25

Three major metabolites (M1, M2, M3) of nomifensine (8-amino-1,2,3,4-tetrahydro-2-methyl-4-phenyl-isoquinoline) are formed by hydroxylation and methoxylation of the phenyl ring. They were compared with nomifensine 1. in various psychopharmacological tests in vivo, carried out in mice after oral or i.p. treatment and 2. in neurochemical in vitro studies, measuring inhibition of noradrenaline (NA), dopamine (DA), and serotonin (5-HT) uptake in rat brain synaptosomes. M1 (4'-hydroxy-nomifensine) was the most active metabolite, while M2 and M3 had little or no effect in pharmacological tests. M1 reversed reserpine hypothermia in doses greater than 2.5 mg/kg, antagonized tetrabenazine catalepsy (ED50 68 mg/kg) and reversed oxotremorine hypothermia (ED50 33 mg/kg). In these tests nomifensine was also active, being about 3-10 times more potent than M1. In contrast to nomifensine M1 had also serotoninergic activity, potentiating both phenelzine-induced twitching (ED50 11 mg/kg) and the anticonvulsant effect of 5-hydroxytryptophan. Moreover, M1 prolonged the hexobarbital sleeping time in doses greater than 10 mg/kg, prevented nicotine-induced convulsions (ED50 58 mg/kg) and reduced the oxotremorine tremor (ED50 59 mg/kg). The LD50 of M1 was 1100 mg/kg orally. In vitro M1 was equipotent with nomifensine in inhibiting DA uptake (IC50 1.5 x 10(-7) M) and twice as active in inhibiting NA uptake (IC50 1.1 x 10(-8) M). In contrast to nomifensine M1 was also a potent inhibitor of 5-HT uptake (IC50 3.3 x 10(-7) M). M2 and M3 were less active than M1 in all experiments.
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PMID:Pharmacological and biochemical studies with three metabolites of nomifensine. 40 62


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