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

The degree of hypothermia elicited by morphine was greater in DBA/2 than C57BL/6 strain mice of both sexes. Hypothermia elicited by morphine was antagonized by naloxone in both strains of mice, suggesting the involvement of opioid receptors. To examine the role of genetic factors in the strain difference of morphine-induced hypothermia, the effect of morphine on changes in the rectal temperature was studied in the 6 generations of male mice, including the 2 inbred strains, P1 (DBA/2) and P2 (C57BL/6), their F1 and F2 hybrids, and 2 backcrosses, B1 (F1 X P1) and B2 (F1 X P2). The order of mean temperature decrease determined 40 min after 20 mg/kg morphine injection was P1 greater than B1 greater than F1 = F2 greater than B2 greater than P2. There was no maternal effect on the morphine responses of the F1 generation. Biometrical analysis revealed that DBA/2 (P1) is partially dominant over C57BL/6 (P2) and contribution of polygenes was suggested.
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PMID:Genetic analysis of hypothermia induced by morphine in two strains of inbred mice. 361 52

The acute effects of diisopropylfluorophosphate (DFP) were assessed in DBA/2Ibg, C57BL/6Ibg and C3H/2Ibg mice. The DFP was administered by intraperitoneal injection in saline. Brain acetylcholinesterase (AChE) activity was maximally inhibited within 5 min after injection. All mice showed signs of organophosphate intoxication including salivation, lacrimation, diarrhea, respiratory distress, tremor and, at high doses, seizures. The C57BL mice were most susceptible to these effects of DFP. The LD50 values for DFP were 8.0, 7.6, and 6.8 mg/kg for male DBA, C3H, and C57BL mice, respectively. The LD50 values for females were nearly the same. Body temperature and brain AChE activity decreased in a dose-dependent manner following injections of DFP of 3.17, 4.22, 5.28, and 6.33 mg/kg. Maximum temperature depression occurred 2 hours after DFP administration; by 24 hours temperatures had returned to normal except for C57BL mice treated with the highest dose of DFP. The C57BL strain was most susceptible to the DFP-induced hypothermia, the C3H strain was the most resistant, and the DBA strain was intermediate. Maximum temperature depression and residual AChE activity, as measured 24 hours after injection, were linearly related. These strain differences do not seem to be explained easily by a differential inhibition of AChE activity.
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PMID:Genetically determined differences in acute responses to diisopropylfluorophosphate. 399 71

The influence of chronic ethanol treatment on synaptosomal plasma membrane (SPM) cholesterol and phospholipid levels was determined in C57BL, Swiss Webster, DBA and BALB-C mice. A significant increase in SPM cholesterol after chronic ethanol treatment was observed only in C57BL mice. No change in either SPM cholesterol or C/P ratios was observed in the other three mouse strains tested, albeit all strains were rendered tolerant to ethanol as judged by ethanol-induced hypothermia, sleep time and blood ethanol upon awakening. It is concluded that an increase in SPM C/P ratio is not a necessary concomitant of behavioral or neurophysiological tolerance resulting from chronic ethanol consumption. In other studies, the possible relationship between SPM C/P ratios and initial neurosensitivity to ethanol was assessed in eight different mouse strains as well as two selected lines of mice. None of the individual mice had been tested previously with ethanol. No meaningful correlations could be made when the SPM C/P ratios of these strains were compared to either ethanol-induced sleep time, blood ethanol upon awakening or hypothermia. Therefore, genetic differences in SPM C/P ratios do not appear to be functionally related to phenotypic initial neurosensitivity to ethanol.
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PMID:Synaptosomal cholesterol and phospholipid levels in several mouse strains differentially sensitive to ethanol. 403 42

DBA mice were fed lab chow containing phenobarbital for seven or eight days. Upon withdrawal of the phenobarbital diet, dependence was evidenced by appearance of hypothermia, handling-induced convulsions and lethal seizures. Functional tolerance was determined by injecting phenobarbital into mice treated with the phenobarbital diet or a pair-fed control diet and measuring the brain concentration of phenobarbital at the time of loss of righting reflex and the time of regaining righting reflex. Both measures demonstrated that chronic consumption of phenobarbital resulted in functional tolerance. When the diet was withdrawn for two days, tolerance was no longer present, indicating a rapid reversal of the adaptive changes. The veratridine-stimulated uptake of 24Na by isolated brain synaptosomes was used as a measure of membrane function. Sodium uptake was inhibited in vitro by pentobarbital and ethanol, and the inhibitory effects of these drugs were attenuated by chronic in vivo phenobarbital treatment. The fluidity of brain synaptic plasma membranes was estimated by the fluorescence polarization of the fluorescent probe molecules 1-(4-trimethylammonium phenyl)-6-phenyl-1,3,5-hexatriene and 1,6-diphenyl-1,3,5-hexatriene. Synaptic membranes from mice treated chronically with phenobarbital did not differ from those of control mice with regard to either the baseline fluorescence polarization of the probes or the decrease in fluorescence polarization produced by in vitro exposure to phenobarbital or ethanol. Taken together, these results indicate that although chronic phenobarbital ingestion resulted in tolerance and dependence (studied in vivo), and adaptation of sodium channels (studied in vitro), there was no evidence that these changes were due to alterations in the membrane physical properties.
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PMID:Barbiturate tolerance and dependence: effects on synaptosomal sodium transport and membrane fluidity. 404 Jun 39

Strain differences in response to the administration of two lethal doses (700 and 900; mg/kg) of lithium chloride were studied in eight week old males from six genetic strains of mice. Two parameters were considered; (a) toxicity (time to death) and (b) hypothermia. Lithium distribution in the body (blood, seven tissues, excreta and urine) were evaluated for each strain following IP injection of 200 mg/kg dose of LiCl. The strain differences were significant for toxicity. The order of susceptibility of the strains was 129/ReJ greater than S.W. greater than C3H/S greater than DBA/2 = Balb/c greater than C57/6J with a 15-fold difference between the most susceptible and the least susceptible strain at the 900 mg/kg dose. Strain differences for hypothermic response at both doses were not significant. Significant strain differences were also observed for lithium distribution in different parts of the body, excreta and urine. The concentration of Li+ found in urine and excreta was positively correlated with resistance (time to death at 900 mg/kg LiCl) to the toxic effect of lithium. The lithium concentration in blood, muscle and lung on the other hand reflected a negative correlation with toxicity. The susceptibility of a strain could be characterized by its inherent lithium excretory ability, particularly through urine. It may suggest an involvement of membrane transport mechanisms in determining toxicity to lithium compounds.
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PMID:Strain dependent rate of Li+ elimination associated with toxic effects of lethal doses of lithium chloride in mice. 631 89

The hypothermic responses of mice that occur after acute injection of nicotine show genetic influences. The body temperatures of mice of all five strains tested decreased after injection of either 0.75 or 1.5 mg/kg nicotine, but mice of the C3H strain were less affected than were those of the DBA, BALB, or C57BL strains. Mice of the A strain were the most sensitive to nicotine's effects. Genetic effects on nicotine-induced hypothermia were further examined using a five-by-five diallel cross. Additive genetic variance occurred at both nicotine doses. Substantial dominance variance, including directional dominance toward a large hypothermic response induced by injection of a low dose of nicotine (0.75 mg/kg), suggested that an intense response to a low drug dose is adaptive. The directional dominance was absent after treatment with a high dose (1.5 mg/kg) of the drug. Epistatic interactions occurring in crosses involving C57BL mice were pronounced.
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PMID:A diallel analysis of nicotine-induced hypothermia. 652 21

To investigate whether genetic factors may play a role in the difference of the responses to morphine between inbred strains of mice, we determined the effect of morphine on the plasma cyclic nucleotides, the motor activity and the rectal temperature in the 2 progenitor strains of mice, DBA and C57BL, their F1 and F2 hybrids, and the 2 backcross progenies between F1 and parental strains. C57BL was partially dominant over DBA concerning the motor activity induced by morphine, whereas DBA was partially dominant over C57BL in terms of the increase in plasma cyclic nucleotides and the hypothermia elicited by morphine. The biometric analysis suggested that the strain difference in the effects of morphine was genetically determined except for plasma cyclic AMP, and that among these quantitative traits, the effects of morphine on motor activity and rectal temperature were controlled by more than one allelic gene pairs.
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PMID:A genetic analysis of morphine responses in mice. 653 Oct 77

Hypothermia was studied 5 min before, and 30 and 60 min after intraperitoneal administration of ethanol (3 g/kg) in 20 inbred strains of mice. Ethanol was given daily for 8 days, and temperatures were taken on Days 1, 3, 5, and 8. Tolerance was indexed by the reduction in hypothermia over days. There were large strain differences in baseline temperature, the hypothermic effect of ethanol, and in development of tolerance to hypothermia. Some strains of mice (DBA/1J, DBA/2N, MA/MyJ, and PL/J) did not develop tolerance to the hypothermic effect of ethanol. Initial sensitivity to the hypothermic effect of ethanol was significantly genetically correlated with tolerance development, indicating control of these responses by common genes. Ethanol-induced changes in activity and ataxia, as well as blood ethanol concentrations, were also assessed. Although there were significant strain differences in activity reduction, ataxia, blood-ethanol concentrations, and changes in these parameters during the course of chronic treatment, none of these variables could explain the genetic differences in hypothermic sensitivity and tolerance.
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PMID:Tolerance to ethanol hypothermia in inbred mice: genotypic correlations with behavioral responses. 675 16

C57B1/6 mouse brain serotonin levels were depleted by feeding animals a diet containing no tryptophan. When such mice were injected with ethanol, they were found to lose their righting reflex for significantly longer periods and to have a lower body temperature than control animals. Animals consuming the diet containing no tryptophan metabolized ethanol more slowly than controls. Although daily injections of kynurenine reinstated ethanol metabolism to normal, the duration of loss of righting reflex and the hypothermia induced by ethanol were unaffected by kynurenine pretreatment. Tryptophan (75 mg/kg) administered six hours prior to ethanol injection returned brain serotonin levels to normal in tryptophan-deprived mice. Mice injected with tryptophan were found to respond to ethanol as did the control animals. When brain ethanol levels were determined at the time the animals lost their righting reflex and when animals regained their righting reflex, tryptophan-deprived mice were found to regain the righting reflex at the same brain ethanol levels as those at which such animals lost their righting reflex. Tryptophan administration to tryptophan-deprived mice resulted in their regaining the righting reflex at higher ethanol levels than those at which they lost the reflex. Similar experiments were carried out on C3H/HeJ and DBA/J2 mice. The results indicate that C3H mice developed some acute tolerance while DBA mice failed to develop any acute tolerance. The possibility exists that the strain difference in the degree of sensitivity to ethanol observed in these mice may be due to differing abilities to develop acute tolerance.
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PMID:Strain differences in the development of acute tolerance to ethanol. 740 84

1. The behavioural and anticonvulsant effects of eight pyrroloimidazopyridines (PI1a-d and PI2a-d) and four pyrrolopurines (PP) were studied after intraperitoneal administration in DBA/2 mice, a strain genetically susceptible to sound-induced seizures. 2. The anticonvulsant effects were evaluated in DBA/2 mice on seizures evoked by means of auditory stimulation (109 dB, 12-16 kHz) in animals placed singly under a perspex dome. 3. Hypothermic activity was observed after the highest doses of the pyrroloderivatives studied. 4. Our study demonstrated that the anticonvulsant effect of pyrroloimidazopyridines (PI1-7,8,8a,9-tetrahydro-6H-pyrrolo-[1',2':1,2]imidazo[4,5-b]pyrid in-6- ones) and pyrrolopurines (PP) was generally better than corresponding pyrrolobenzimidazoles (PB) and pyrroloimidazopyridines (PI2-5,5a,6,7-tetrahydro-8H-pyrrolo[2',1':2,3]imidazo[4,5-c]pyridin-8- ones) and, in some cases, comparable to that of phenytoin and desmethylclobazam. 5. The anticonvulsant potency of the derivatives studied cannot be directly related to their lipophilicity.
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PMID:Anticonvulsant activity of pyrrolo[1',2':1,2]imidazo[4,5-b]pyridines, pyrrolo[2',1':2,3]imidazo[4,5-c] pyridines and pyrrolo[2,1-f]purines in DBA/2 mice. 783 20


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