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

These studies were designed to determine several, possibly related, physiological correlates of an acute dose of ethanol. Male rats were injected with 0.5, 1.0, or 2.5 g/kg of ethanol intraperitoneally, and the accumulation of newly synthesized labeled norepinephrine (from 3H-tyrosine) and of labeled norepinephrine metabolites was examined in several brain regions. Ethanol treatment increased labeled norepinephrine and decreased norepinephrine metabolities in the hypothalamus, brain stem plus midbrain, and telencephalon, without altering endogenous norepinephrine levels. A time course, selected on the basis of previous behavioral studies (Jaffe and Pohorecky, submitted manuscript) on the effects of ethanol on central noradrenergic neurons, disclosed that the accumulation of labeled norepinephrine metabolites was higher than that in saline-injected controls from 30-60 minutes after ethanol injection in the brainstem plus midbrain area, while between 5 and 35 minutes levels were lower than those in control animals. Plasma corticosterone levels were highest 30 minutes after saline injection, while in the ethanol group (1 g/kg) steroids were highest 60 minutes after the injection. Body temperature was significantly decreased only by the 2.5 g/kg dose of ethanol; the hypothermia became evident 50 minutes after an injection of this dosage. We conclude that the brief hypermotile stage produced by a 1 g/kg dose of ethanol (Jaffe and Pohorecky, submitted manuscript) is possibly related to the increased synthesis and release of norepinephrine from central noradrenergic neurons.
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PMID:Noradrenergic involvement in the acute effects of ethanol. 119 25

Changes in rectal and skin temperatures following intraventricular injection of biogenic amines and related substances were investigated in rats. Intraventricular injection of norepinephrine in a small dose (6 mug) produced a slight elevation of rectal temperature, but in larger amounts (25-50 mug) resulted in a dose-dependent hypothermia which was associated with a marked rise of skin temperature. No change was observed in plasma free fatty acid and glucose levels and oxygen consumption after intraventricular injection of norepinephrine (25 mug). Intraventricular injection of imipramine and safrazine produced a slight fall in the rectal temperature. Norepinephrine-induced hypothermia was more pronounced in rats pretreated with safrazine and less in rats pretreated with alpha-methyl-p-tyrosine, as compared with that in controls. Intraventricular injection of 6-hydroxydopamine (0.75-250 mug) brought about a marked dose-dependent hypothermia. The second injection of 6-hydroxydopamine 5 days after the first injection had no effect on the body temperature. Norepinephrine injection 2 days after the second injection of 6-hydroxydopamine produced a more pronounced hypothermia than the change in control rats without pretreatments. Haloperidol did not affect the hypothermia induced by 6-hydroxydopamine. Intraventricular injection of dopamine and L-DOPA showed less effect that norepinephrine had. Intraventricular injection of phenoxybenzamine prior to norepinephrine blocked the hypothermia and skin temperature elevation which are normally observed following norepinephrine injection, while propranolol given in the same way showed less or no effect. Intraventricular injection of phenylephrine produced a dose-dependent hypothermia, whereas no dose-response relationship was obtained by isoproterenol. These results suggest that in the rat the hypothermic effect of norepinephrine injected intraventricularly is mediated by an action of central alpha-receptor. At high and low ambient temperatures hypothermia was similarly observed following intraventricular injection of 5-hydroxytryptamine (25 mug) as at normal room temperature. On the other hand, norepinephrine (25 mug) produced a rise in rectal temperature at high ambient temperature and a marked fall at low ambient temperature. The hypothermic effect of norepinephrine was not different between cold-adapted ones at room temperature. From the results the role of norepinephrine and other biogenic amines in the brain in thermoregulatory processes was discussed.
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PMID:[Role of brain biogenic amines in the central thermoregulatory mechanism of the rat (author's transl)]. 124 80

Beta-phenylethylamine on injection into mice (100 mg/kg i.p.) produces a marked hyperthermia which is followed by a prolonged hypothermia. The hyperthermic response was studied in this report. The hyperthermic response was inhibited by p-chlorophenylalanine, methysergide, cyproheptadine, alpha-methyl-tyrosine, propranolol, practolol, phenoxybenzamine, phentolamine, haloperidol, pimozide, protriptyline and desipramine. Lysergic acid diethylamide potentiated the response, while p-chloroamphetamine was without effect. While FLA-63 potentiated the response, disulfiram and reserpine were ineffective in preventing the hyperthermia. Nicotinic acid and prostaglandin E1 did not prevent PE induced hyperthermia. It was concluded from these results that PE induced hyperthermia in mice is blocked by agents that reduce the effective concentration of either DA or 5-HT in the central nervous system (by either synthesis inhibitors or receptor blockers). The involvement with catecholaminergic neurons at least was postulated to be a result of PE induced release of DA from DA neurons.
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PMID:The effect of beta-phenylethylamine on temperature in mice and its possible mechanisms of action. 124 22

The effects of different dopamine (DA) D2 receptor agonists and the DA D2 receptor antagonist, emonapride, on body temperature were studied in male mice. The aim of the study was to test whether DA D2 receptor agonists ranging from full agonists to agonists with low efficacy could be differentiated by means of their effect on body temperature. Talipexole induced a marked hypothermia (maximum decrease of 6.5 degrees C). Apomorphine, quinelorane, (+)-4-propyl-9-hydroxy-naphtoxazine((+)-PHNO), and (-)-N-n-propylnorapomorphine ((-)-NPA) induced a maximum hypothermia of 3.5-4.1 degrees C. Quinpirole and (+)-3-(3-hydroxyphenyl)-N-n-propylpiperidine ((+)-3-PPP) induced a less pronounced hypothermia (1.7 and 1.5 degrees C), and preclamol ((-)-3-PPP), terguride and 3-(4-(4-phenyl-1,2,3,6-tetrahydropyridyl)-(1))-butyl)-indole (EMD 23448) had no or only a slight effect. Emonapride induced significant hyperthermia at high doses. Apomorphine-, quinelorane- and talipexole-induced hypothermia was reversed by terguride and preclamol, whereas EMD 23448 partially reversed the apomorphine-induced hypothermia. The alpha 2-adrenoceptor antagonist, idazoxan, partly reversed the effect of talipexole. Quinpirole had no effect on the hypothermic effect of the above-mentioned agonists. Pretreatment with the catecholamine synthesis inhibitor, alpha-methyl-m-tyrosine, increased significantly the hypothermic response to quinpirole, whereas the effect of quinelorane was unchanged. It is suggested that the effect of DA D2 agonists on body temperature in mice can be used to differentiate between agonists with different efficacies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects on body temperature in mice differentiate between dopamine D2 receptor agonists with high and low efficacies. 135 51

The effects of dermorphin on EEG and autonomic variables are compared with the effects of 2 analogues and 2 homologues, all administered intracerebroventricularly in the rabbit. Dermorphin was the most effective in modifying all considered parameters: increase of cortically derived and calculated total power, bradycardia, respiratory depression and hypothermia. The dibenzylated heptapeptide was essentially inactive. The electrocortical pattern induced by the administration of L-dermorphin suggests a functional correlation between the amino acid D-ala 2 and the effects on EEG. Comparison between the effects produced by the N-terminal tetrapeptide and pentapeptide led us to hypothesize that amino acid Tyr 5 may be specifically involved in inducing the autonomic effects.
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PMID:Quantitative EEG and autonomic patterns of synthetic peptides related to dermorphin. 136 72

We recently reported that H-Lys psi (CH2NH)Lys-Pro-Tyr-Ile-Leu-OH (JMV 449), a pseudopeptide analogue of neurotensin-(8-13) with a reduced CH2NH bond in position 8-9, was about 3 times more potent than neurotensin in binding to mouse brain membranes and in contracting the guinea-pig ileum, and was markedly more resistant to degradation than neurotensin when exposed to rat brain membranes. In the present study, we compared the time courses and dose-response relationships for the ability of i.c.v. injected neurotensin and JMV 449 to elicit hypothermia and analgesia (tail-flick test) in the mouse. The results show that the pseudopeptide analogue behaved as a highly potent and long-lasting neurotensin agonist in these two in vivo bioassays. The analogue should prove very useful for studying the effects of chronic neurotensin receptor stimulation in vitro and in vivo.
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PMID:JMV 449: a pseudopeptide analogue of neurotensin-(8-13) with highly potent and long-lasting hypothermic and analgesic effects in the mouse. 142 58

A study was conducted to investigate changes in monoamine metabolism in the brain of rats with acute ischemic hepatic failure (AHF) induced by two-stage hepatic devascularization. Strict artificial cardiopulmonary management was used to exclude possible confounding effects of hypotension, hypothermia and hypoxemia that often appear in AHF. Rats were put in an incubator at 34 degrees C before the ligation of the hepatic artery (second stage operation), tracheotomized and ventilated artificially throughout the remaining experimental periods. No significant difference was observed in physiological parameters, including body temperature, pulse rate and systolic arterial blood pressure or PaO2 between AHF and sham operated rats. Brain levels of norepinephrine (NE) and its metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG), dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanilic acid (HVA), and serotonin (5-hydroxytryptamine, 5HT) and its metabolite 5-hydroxyindoleacetic acid (5HIAA) were determined by HPLC-voltametry. AHF rats showed significantly higher MHPG, DOPAC, 5HIAA and lower NE levels in the brain compared to controls. In addition, a significant negative correlation between NE and tyrosine (Tyr), a significant positive correlation between MHPG and Tyr or phenylalanine (Phe), and a significant positive correlation between DOPAC and Tyr or Phe were observed. In conclusion, the changes in monoamine metabolism in the brain of AHF rats are clearly induced specifically by hepatic failure itself, possibly through an altered metabolism of amino acids.
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PMID:Changes in brain monoamine metabolism in rats with acute ischemic hepatic failure under artificial cardiopulmonary management. 157 24

1. Administration of bromocriptine (0.1-2.5 mg/kg, i.p.) to mice produced hypothermia. 2. Pretreatment with the alpha 1-adrenoceptor blocker, prazosin (2.0 mg/kg, i.p.) or the alpha 2-adrenoceptor antagonist yohimbine (2.5 mg/kg, i.p.) had no effect on this response. 3. The inhibitor of catecholamine synthesis, alpha-methyl-p-tyrosine, and the muscarinic antagonist, atropine (10 mg/kg, i.p.) failed to alter the hypothermia. 4. Pretreatment with the dopamine (DA) receptor antagonists haloperidol (0.02 mg/kg, i.p.) or cis-flupenthixol (0.01 mg/kg, i.p.) completely blocked this response while trans-flupenthixol (0.05 mg/kg, i.p.) was inactive. 5. Depletion of 5-HT in the brain by p-chlorophenylalanine reduced the hypothermic response. 6. Similarly, pretreatment with the serotonergic (5-HT) receptor blocker ketanserin (1 mg/kg, i.p.) attenuated the hypothermia and at a dose of 2 mg/kg (i.p.) it completely blocked the hypothermic response. 7. Methysergide (5 mg/kg, i.p.) was also effective in antagonizing the hypothermia. 8. It was concluded that both DA and 5-HT mechanisms are involved in bromocriptine-induced hypothermia in mice.
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PMID:Bromocriptine-induced hypothermia in Balb/C mice: its possible mechanism of action. 165 Dec 67

In order to re-evaluate the role of two putative waking systems, we injected a neural cell body toxin, ibotenic acid (IA) (45 micrograms/microliters), into the mesencephalic reticular formation (MRF) and/or the posterior hypothalamus (PH). On the one hand, when the cell body destruction was only restricted to the MRF, the IA microinjection was followed by a temporary high voltage and slow neocortical electroencephalogram (EEG) during the first 24 postoperative hours and by a subsequent long term increase in waking which lasted 8-12 h. After the first postoperative day, there were no motor disturbances, no aphagia nor adypsia, no alteration of cortical activation and no modification of thermoregulation or of the sleep-waking cycle. On the other hand, the IA microinjection into the PH induced a hypothermia during the first postoperative night and a dramatic transient hypersomnia immediately after the disappearance of the anesthesia (14-24 h after the IA injection). On the third day, all cats recovered control level of paradoxical sleep (PS), slow wave sleep (SWS) and cerebral temperature. They presented normal motor behavior but they were not able to eat by themselves during the first postoperative week. Finally, when the lesions of the MRF and the PH were realized in one single operation, the cats were first motionless in a comatose state for 2-3 days. This state was accompanied by a transitory hypothermia and the suppression of a spontaneous or evoked cortical low voltage fast activity. However, from the 2nd postoperative week, both behavioral and EEG waking re-occurred. By contrast, the two successive operations (MRF followed by PH) did not induce a comatose state. We did not observe any deficit in motor behavior, and the sleep-waking cycle was quite normal as from the second postlesion day. In the MRF-PH-lesioned cats, the injection of alpha-methyl-p-tyrosine (150 mg/kg) induced a large decrease in waking and a moderate increase in PS. In the MRF-lesioned cats, IA produced a large area of cell body loss, centered in the MRF, that extended from levels A2 to A6 of stereotaxic planes and sometimes encroached upon the red nucleus and the substantia nigra. In the PH-lesioned cats, the histological analysis revealed a great loss of cell bodies in the PH extended from levels A8 to A12.5. The damage included the lateral and posterior hypothalamic areas and sometimes the tuberomamillary nucleus. In MRF- and PH-lesioned cats, the cell body loss extended from levels A2 to A12.5.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotoxic lesion of the mesencephalic reticular formation and/or the posterior hypothalamus does not alter waking in the cat. 167 7

Choroid plexuses from the lateral (LVCP) and fourth ventricles (FVCP) of rats or rabbits were incubated in artificial cerebrospinal fluid (CSF) containing 1 microM [14C]L-carnitine with various concentrations of L-carnitine ranging from 0.01 mM to 1.0 mM. The time course of 1 microM [14C]L-carnitine uptake by the choroid plexus indicated that it increased linearly for the first 15 min. Steady-state levels were reached by 30 min with tissue concentrations more than 20 (FVCP)- to 30 (LVCP)-fold greater than the concentration in the medium. The uptake of [14C]L-carnitine was increased with increasing concentrations of the substrate in the medium and this uptake followed Michaelis-Menten kinetics. The uptake by the rat choroid plexus took place against a concentration gradient via a saturable process and kinetic analysis revealed Km of 32 microM (LVCP) and 34 microM (FVCP) and Vmax of 21 (LVCP) and 17 nmol/ml/min (FVCP), respectively. Ouabain inhibited the uptake by 51% (FVCP) and 48% (LVCP) and hypothermia (0 degrees C) produced inhibition by 97% (FVCP) and 96% (LVCP), respectively. However, the uptake of L-carnitine was not sensitive to probenecid or tyrosine, which indicates the presence of an independent carrier for L-carnitine in the choroid plexus. Similar results were obtained with the rabbit choroid plexus.
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PMID:Kinetic analysis of L-carnitine uptake by the choroid plexus. 193


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