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

The effect of ethanol and pentobarbital on in vivo tryptophan hydroxylase activity and its relationship to drug-induced alterations of thermoregulation was examined in long-sleep (LS) and short-sleep (SS) mice. Serotonin function was measured in both the presence and absence of ethanol or pentobarbital in six discrete brain regions. Differences in basal levels of serotonin, 5-hydroxyindole acetic acid or in vivo tryptophan hydroxylase (TpH) activity were found only in the hypothalamus and dorsal raphe nuclei (SS slightly higher). Ethanol (4.2 g/kg i.p) caused significant reductions in in vivo TpH activity in the dorsal and pontine-medullary raphe nuclei and hypothalamus (putative thermoregulatory areas) in both LS (50-60% decrease) and SS (15-30% decrease) mice, but it had no effect on TpH activity in the striatum, cortex or hippocampus. The greater degree of ethanol-induced reduction in TpH activity in LS mice was associated with a greater degree of hypothermia (LS, 4.2 degrees C vs SS, 2.0 degrees C). Pentobarbital had equivalent effects in LS and SS mice on TpH activity in central nervous system thermoregulatory areas (decreases of 40-60%) and on body temperature (decreases of 6.8-7.5 degrees C). When the mice were given ethanol at an elevated environmental temperature (34 degrees C) the hypothermia was almost abolished completely, but depressant effects on TpH activity remained, suggesting that ethanol-induced decreases in TpH activity were direct effects and not secondary to hypothermia. Alterations in ethanol or pentobarbital elimination did not appear to account for the observed differences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serotoninergic involvement in ethanol-induced alterations of thermoregulation in long-sleep and short-sleep mice. 194 31

The alteration of monoamines and their metabolites in the brain in response to hypothermia was studied using rats subjected to a cold and immobilization stress. The experiments were designed to compare the responses in the "hypothermal" rats with those in the "normothermal" ones which received the same stress except for the change in body temperature. It has been found that the contents of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in various cerebral regions were significantly decreased during hypothermia. These decreases were readily reversed by the rewarming of animals. Moreover, the increase in the content of 5-hydroxyindole-3-acetic acid (5-HIAA), the metabolite of 5-HT, was also detected in some cerebral regions where the decrease of 5-HT was observed. Although the dopamine (DA) contents in all cerebral regions examined were found to be unaltered, its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and/or homovanillic acid (HVA) contents in most regions in the brain showed a significant elevation during and/or after the occurrence of hypothermia. These results suggest that the metabolic turnovers of 5-HT and DA in various cerebral regions may be accelerated during hypothermia.
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PMID:Alteration of the turnover of dopamine and 5-hydroxytryptamine in rat brain associated with hypothermia. 241 47

Beraprost sodium (sodium (+/-)-(1R*,2R*,3aS*,8bS*)-2,3,3a,8b-tetrahydro-2- hydroxy-1-[(E)-(3S*)-3-hydroxy-4-methyl-1-octen-6-ynyl]-1H- cyclopenta[b]benzofuran-5-butyrate, TRK-100) is an orally active epoprostenol (prostaglandin I2, PGI2) analogue. Its effect on the central nervous system (CNS) was studied. 1. When orally administered in mice, beraprost sodium at 0.3 mg/kg caused a flush of skin, a suppression of spontaneous motility, and a fall of body temperature. At 1 mg/kg and more, it showed obvious sedation, prolongation of hexobarbital hypnosis, and analgesic action in acetic acid-induced writhing test. However, even at 3 mg/kg beraprost sodium neither induced ataxia nor had anticonvulsant activity. Hypothermia was also observed in rabbits at 1 mg/kg (p.o. and i.v.). 2. When intravenously administered, beraprost sodium exerted long-lasting action on the CNS, while its pharmacological effects resembled those of PGI2. 3. Oral administration of beraprost sodium did not inhibit aggregation toxicity induced by methamphetamine (20 mg/kg i.p.) in mice. Beraprost sodium at doses higher than 1 mg/kg enhanced aggregation toxicity induced by methamphetamine (5 mg/kg i.p.), while intracerebral ventricular administration of beraprost sodium failed to enhance it. 4. In rat spinal reflex, intravenous administration of beraprost sodium (0.1 mg/kg) slightly enhanced monosynaptic reflex and at a high dose (1 mg/kg) suppressed polysynaptic reflex. 5. In the rabbit EEG, intravenous administration of beraprost sodium at a high dose (1 mg/kg) showed some effects such as the continuous pattern of wakefulness and a fall in power of the EEG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacology of beraprost sodium. 1st communication: effect on the central nervous system. 251 Jul 42

In the early 1970's, calcium ions were implicated in the mechanism underlying the perturbation of the "set point" for body temperature produced by a thermolytic drug. Since Ca++ is thought to be involved in the incapacitating effects of ethanol on body temperature and motor coordination, this investigation sought to compare the differential central actions of a Ca++ chelating agent with those of a Ca++ channel antagonist on ethanol-induced poikilothermia and motor functions. A chronically indwelling cannula for intracerebroventricular (ICV) injection was implanted stereotaxically in each of 25 adult male Sprague-Dawley rats. Following postoperative recovery, each rat was given ethanol in a 20% v/v solution by the intraperitoneal route in a dose of 4.0 g/kg, which was selected to insure a clear-cut impairment of autonomic and motorial functions. Colonic temperature, behavioral sleep, righting reflex and degree of motor coordination on a rotorod were monitored at selected intervals for 5.0-7.0 hr after the injection of ethanol. Two experimental designs were used: First, either 12.5, 25 or 50 micrograms ethyleneglycol-bis-(beta-amino ethyl ether) N,N'-tetra-acetic acid (EGTA), or 25 or 50 micrograms verapamil, both dissolved in an artificial CSF vehicle, were infused ICV at the same time as ethanol's administration. In the second design, the compounds were infused at the nadir of the ethanol-induced temperature decline. EGTA infused ICV in the rat together with ethanol produced a dose-dependent inhibition of ethanol hypothermia and a more rapid recovery of the animal's righting reflex, arousal and motor coordination than that following ethanol alone. Although verapamil infused ICV in the 50 micrograms but not 25 micrograms dose minimized the poikilothermic response to ethanol, it was not as efficacious as that of EGTA. When infused ICV at the point of maximum fall in the rats' temperature. EGTA entirely reversed the hypothermia induced by ethanol and evoked a thermogenic response in the rat. In contrast, verapamil infused ICV in the same doses tended only to retard the further decline in the animal's body temperature. Similarly EGTA was far more effective than verapamil in ameliorating the other physiological actions of ethanol in terms of the reversal of areflexia, behavioral sleep and motor incoordination. These results suggest that the characteristic attributes of membrane Ca++ in terms of its binding and other neuronal properties play a significant functional role in the incapacitating action of ethanol on the diverse physiological processes mediated by the brain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alcohol-induced poikilothermia, sleep and motor impairment: actions on brain of EGTA and verapamil. 251 53

Effects of 1-(2-ethoxyethyl)-2-(4-methyl-1-homopiperazinyl)benzimidazole difumarate (KB-2413) on the central nervous system were compared with those of ketotifen and chlorpheniramine. Among the various activities related to the central nervous system, KB-2413 showed inhibitory effects on locomotor activity, acetic acid-induced writhing in mice and reserpine-induced hypothermia in rats at a high dose such as 100 mg/kg p.o. However, in mice, it (10-100 mg/kg p.o.) exerted no significant influence on muscle tone, various experimental convulsions, oxotremorine-induced tremor, physostigmine-induced mortality or hexobarbital-induced sleep, and in rats, it had no effect on rectal temperature or conditioned avoidance. It also did not affect spontaneous electroencephalogram (EEG), EEG arousal responses or photic driving response in rabbits at 5 mg/kg i.v. On the other hand, ketotifen and chlorpheniramine affected more widely and strongly the central nervous system than KB-2413. In conclusion, KB-2413 showed a less potent effect on the central nervous system than ketotifen and chlorpheniramine, and no results suggested serious side effects of KB-2413.
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PMID:General pharmacology of 1-(2-ethoxyethyl)-2-(4-methyl-1-homopiperazinyl)benzimidazole difumarate. 1st communication: effects on the central nervous system. 289 9

We studied the in vivo pharmacology of a selective agonist (DPDPE) and a selective antagonist (ICI 174864) at delta opioid receptors. ICI 174864 (10 micrograms icv) caused postural abnormalities, barrel rotation and hypothermia in rats. DPDPE induced behavioural arousal (at 75 micrograms icv) and barrel rotation (at 125 micrograms) in rats. ICI 174864 (10 micrograms icv) attenuated acetic acid induced writhing in mice. This action was antagonized by naloxone (10 but not 2 mg/kg s.c.). A lower, non-agonist dose of ICI 174864 (5 micrograms) antagonized DPDPE (3 micrograms icv) in this test without affecting DAGO (0.0006 micrograms icv), a selective agonist at mu receptors. In the mouse tail flick test, ICI 174864 (10-50 micrograms icv) did not significantly antagonize the agonist actions of DPDPE (40 micrograms icv) or DAGO (0.3 micrograms icv). At 10-50 micrograms icv, ICI 174864 had no marked effect on gastrointestinal transit in mice. ICI 174864 (25 micrograms icv or 20 mg/kg s.c.) did not interact with mu opioid receptors in mice rendered physically dependent on morphine.
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PMID:Studies in vivo with ICI 174864 and [D-Pen2, D-Pen5]enkephalin. 298 31

General pharmacological properties of two kinds of Senso-containing drugs were studied. There were no prominent differences in the pharmacological profile between the two prescriptions. Inhibition of writhing (60 mg/kg, p.o.), prolongation of hexobarbital-induced hypnosis, hypothermia, antipyretic effect, and inhibition of acetic acid-induced capillary permeability (600 mg/kg, p.o.) in mice were observed after administration of these drugs. These effects were suggested to originate from cinobufagin, a constituent of Senso. Augmentation of blood sugar level and inhibition of gastric juice secretion (600 mg/kg, p.o.) in rats were also observed after administration of these drugs. These effects were suggested to originate from constituents of Senso other than cinobufagin. Isolated ileum and aorta of guinea pigs and vas deferens and fundus strip preparation of rats contracted, and isolated trachea of guinea pigs relaxed after the application of these drugs. The majority of these effects were suggested to originate from epinephrine-like or serotonin-like compounds, constituents of Senso.
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PMID:[Pharmacological studies of Senso (Ch'an Su) containing drugs]. 308 46

The effects of 1-[(S)-3-acetylthio-2-methylpropanoyl]-L-prolyl-L-phenylalanine (alacepril, DU-1219), an orally active angiotensin converting enzyme inhibitor, on the central nervous and sensory systems and on several other functions were compared with those of captopril in the experimental animals. Alacepril at the high oral dose of 600 mg/kg prolonged the hexobarbital sleeping time and potentiated the reserpine-induced hypothermia in mice. However, alacepril at the same dose did not affect the general behavior, convulsions induced by maximal electroshock, pentetrazol and strychnine, active avoidance in mice and body temperature in rats. In addition, alacepril (200 mg/kg i.v.) has little effect on general behavior in mice. Captopril at over 107 mg/kg p.o. produced eyelid closure and at 320 mg/kg prolonged the hexobarbital sleeping time. A metabolite of alacepril, desacetylalacepril (DU-1227) (200 mg/kg i.v.), caused salivation in mice. Alacepril and DU-1227 at 60 mg/kg i.v. were without effect on flexor reflex and spontaneous electroencephalogram (EEG) in cats, while captopril at the equimolar dose depressed the flexor reflex and showed a tendency to increase the beta 2-band relative power of the cortical EEG. Alacepril and captopril neither affected the writhing syndrome induced by acetic acid nor that by phenylquinone in mice. Local anesthetic and irritant activities in rabbits and effect on neuromuscular junction in anesthetized rats were not observed with the two compounds. Alacepril at the oral dose of 0.1 mg/kg potentiated the carrageenin-induced edema in rats. However, the effect was one third that of captopril. Alacepril and captopril did not affect the increased vascular permeability by acetic acid in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacology of the novel angiotensin converting enzyme inhibitor alacepril. 2nd communication: Effects on central nervous and sensory systems and on the other functions. 351 78

Antagonists of the norepinephrine reuptake and beta-adrenoreceptor agonists are potent, at once, on the three following tests: antagonism of hypothermia induced by reserpine, oxotremorine and apomorphine. 2-Carboxy-4-isopropenyl-3-pyrrolidine-acetic acid (kainic acid), which is a powerful stimulant of the neurons and a destroyer of the dopaminergic neurons, has been used in these tests to show if it is possible to antagonize hypothermia induced by different substances. The results obtained show that kainic acid is potent on these three tests, thus providing evidence that it is a stimulant of norepinephrine neurons as well as serotoninergic neurons, even if it is peripherically injected.
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PMID:Effects of kainic acid on hypothermia induced by reserpine, oxotremorine and apomorphine in mice. 359 46

General pharmacological properties of cinobufagin (CB), isolated from Senso, were compared with those of digitoxin (DT). Decrement of spontaneous movement, inhibition of writhing, prolongation of hexobarbital-induced hypnosis, muscle relaxation, inhibition of acetic acid-induced capillary permeability, hypothermia, antipyretic effect in mice; excitation of respiration in rabbits; nerve blocking action in the isolated sciatic nerve of frogs; cardiotonic effect in the isolated atria of guinea pigs; contraction of the isolated ileum of rabbits and guinea pigs; contraction of the aorta of guinea pigs; and relaxation of the isolated trachea of guinea pigs were common properties observed after separate application of CB and DT. Membrane stabilizing effect in erythrocytes of rats and inhibition of propulsive motility of the small intestine in mice were observed only after the application of CB. Inhibition of gastric juice secretion, antiinflammation on carrageenin- or dextran-induced edema, diuresis in rats, mydriasis in mice and potentiation of transmission in the neuromuscular junction of rats were observed only after the application of DT. After oral administration, the onset of the effects of CB (30 min) was faster than that of DT (3-4 hr), and the duration of the effects of CB (1-2 hr) was shorter than that of DT (greater than 24 hr).
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PMID:[Pharmacological studies of cinobufagin, in comparison with digitoxin]. 387 19


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