Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circadian rhythms of core body temperature and general activity in Sprague-Dawley rats were monitored for 21 days using remote radiotelemetry to examine acute and sustained effects of 0 (saline) 1.0, and 2.0 g/kg ethanol injections administered at four different times of day. Ethanol produced dose-dependent and statistically significant hypothermia and hypoactivity when injected at 0100, 0700, 1300, and 1900 h; however, the magnitude of the hypothermic effect was greatest at the 1900-h injection time. Cosinor analyses revealed persistent alterations in both activity and temperature rhythms, which lasted for at least 48 h postinjection. Ethanol significantly shortened the period of activity rhythms when injected in either 1.0 or 2.0 g/kg doses at 0700 and 1300 h, and produced similar period-shortening effects on temperature rhythms at 1300 and 1900 h. The acrophase of the activity rhythm was significantly phase delayed by 1.0 g/kg ethanol at 0700 h, while the acrophase of temperature was significantly phase advanced by 2.0 g/kg ethanol at 0100 h, but significantly phase delayed by the same dose administered at 1300 h. A statistically significant and dose-dependent reduction in the amplitude of the body temperature rhythm was observed at the 1900-h administration time. There were no differences in the MESOR (Midline Estimating Statistic of Rhythm; i.e., rhythm-adjusted mean value) of either temperature or activity circadian rhythms as a function of ethanol treatment at any dose.
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PMID:Phase-response curve for ethanol: alterations in circadian rhythms of temperature and activity in rats. 976 65

1. The main objective of the present study was to investigate the temperature dependence of the cardiac inotropic effects of lignocaine and ethanol (EtOH). 2. We studied the in vitro inotropic actions and interactions of EtOH (2.4 g/L) and lignocaine (25 mg/L) on rat papillary muscles superfused with Tyrode's solution and stimulated at 1 Hz at either 37 or 30 degrees C. Peak tension developed (PTD), maximum velocity of development of tension (VmaxT) and time to peak tension (TPT) were measured. 3. At 37 degrees C, EtOH depressed PTD, while VmaxT and TPT remained unchanged. At 37 degrees C, lignocaine alone or in combination with EtOH depressed all three parameters. 4. At 30 degrees C, EtOH did not modify PTD or VmaxT, whereas TPT decreased. At 30 degrees C, lignocaine decreased TPT, but VmaxT did not change and the effect of lignocaine on PTD was smaller at 30 degrees C than at 37 degrees C. Ethanol and lignocaine in combination decreased all three parameters at 30 degrees C. However, the depression of VmaxT by the combination of lignocaine and EtOH was less at 30 degrees C than at 37 degrees C. 5. Hypothermia (30 degrees C) protected the myocardium against the depressant actions of EtOH and lignocaine, alone or in combination. With EtOH alone, the protection resulted in no change in PTD. When lignocaine was involved, the protection resulted in a weaker action on PTD and VmaxT. The temperature dependence of the action of lignocaine may explain, at least in part, the development of ventricular failure in cardiac surgical patients exposed to lignocaine during hypothermia and rewarming.
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PMID:Temperature-dependent inotropic effects of lignocaine and ethanol on rat heart papillary muscles. 980 63

The influence of deficiency of monoamine oxidase A (MAO A) gene and the lack of enzyme MAO A on the behavior of transgenic mouse strain (Tg8) was studied. It was shown that MAO-A-lacking mice differed from mice of the wild-type strain C3H/HeJ (C3H) by an attenuated acoustic startle response, prepulse inhibition (PPI) was unchanged. In Tg 8 mice, the exploratory nose-poking in the holeboard test as well as exploratory line crossing in the "light-dark" test were decreased. No effect of MAO A deficiency on locomotor activity was found. No alcohol preference or difference between Tg8 and C3H in ethanol consumption in the free-choice test has been found, although an increase in alcohol tolerance has been demonstrated. Ethanol-induced (0.3 g/100 g ip) sleep latency was longer, duration of sleep was shorter and ethanol hypothermia was reduced in MAO-A-lacking mice. Comparison of effects of MAO A knockout with those of irreversible MAO A inhibitor clorgyline (5 and 10 mg/kg ip) on C3H mice showed a similar reducing effect on ethanol-induced sleep, but potentiated ethanol-induced hypothermia. Clorgyline administration provoked a tendency to decrease of exploratory activity in the nose-poking test and decreased the frequency of exploratory rearings in the light-dark test. Clorgyline (5 and 10 mg/kg) did not affect the acoustic startle response, but a dose of 5 mg/kg diminished PPI. Therefore, Tg8 mice exhibited a decreased startle response and exploratory activity and an increased tolerance to ethanol. A similar increase in tolerance to ethanol-induced sleep and a tendency to decrease exploratory behavior were displayed by clorgyline. Other effects on behavior were different, suggesting the influence of long-lasting action of MAO A knockout and the involvement of a compensatory mechanism in Tg8 mice.
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PMID:Altered behavior and alcohol tolerance in transgenic mice lacking MAO A: a comparison with effects of MAO A inhibitor clorgyline. 1116 62

The present study examined the effects of ethanol and naltrexone hydrochloride (a nonselective opiate receptor antagonist) on flash-evoked potentials recorded from both the visual cortex (VC) and the superior colliculus (SC) of chronically implanted hooded rats. There were four treatment conditions administered on separate days: Either saline or naltrexone (10 mg/kg; volume of 1.0 ml/kg) was given 10 min before either saline or ethanol (2.0 g/kg; 20% ethanol solution in a volume of 1.26 ml/100 g). Evoked potentials were recorded 15 min after the intraperitoneal injections were completed. Animals were tested at 23.1 degrees C room temperature. In the VC, ethanol significantly decreased the amplitude of components N1, P3, and N3, whereas it increased the amplitude of P2. Components P1 and N2 were unaffected by ethanol treatment. The SC components P3 and N4 were reduced in amplitude by ethanol, but component P1 was not altered. Latencies of all components in both structures were increased by ethanol. Naltrexone alone did not significantly affect the potentials, nor did naltrexone pretreatment significantly alter the effects of ethanol on the potentials. Naltrexone produced a modest hypothermia of about 0.25 degrees C, whereas ethanol resulted in hypothermia of about 1.0 degrees C. Ethanol, either alone or in combination with naltrexone, significantly reduced body movement during the evoked-potential recording sessions. The results indicate that endogenous opioid systems do not play a major role in the acute effects of ethanol on flash-evoked potentials recorded from primary areas of the visual system.
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PMID:Effects of ethanol on flash-evoked potentials of rats: lack of antagonism by naltrexone. 1166 14

The interaction of mianserin with ethanol in central nervous system (CNS) was investigated. Mianserin was administered at a single dose of 5 or 20 mgkg(-1) i.p. or as daily injections in a dose of 2.5 mgkg(-1) given for 14 days. The influence of mianserin on acute ethanol toxicity (LD(50)), on ED(50) of ethanol in rota-rod test, on the duration of ethanol sleeping time as well as on spontaneous locomotor activity and ethanol-induced hypothermia was investigated. Moreover, the influence of mianserin administered in a dose of 10 mgkg(-1) i.p. on post-ethanol changes in the bioelectric brain activity (EEG) recordings in rabbits was also investigated. The electrodes were implanted into midbrain reticular formation (MRF), dorsal hippocampus (Hp) and frontal cortex (C). Mianserin administered as a single dose of 5 mgkg(-1) was found to decrease LD(50) of ethanol and its ED(50) in rota-rod test. Mianserin administered as a single dose of 5 or 20 mgkg(-1) prolongs ethanol sleeping time in mice but given daily for 14 days has no influence on this time. Mianserin-induced hypothermia was observed after administration of single dose as well as increase of ethanol-induced hypothermia after administration of higher dose (20 mgkg(-1)). Mianserin administered daily for 14 days had no influence on post-ethanol changes in body temperature. Single dose of mianserin 20 mgkg(-1) decreases locomotor activity in mice while repeated administration has no influence on locomotor activity. In contrast, both single dose and repeated administration of mianserin prevents increased locomotor activity of animals observed after ethanol (2.5 mgkg(-1)). Mianserin administered to rabbits (10 mgkg(-1)) induces increase of share of low frequency 0.5-4 cps and decrease of share of frequencies 4-7 and 7-10 cps in EEG recordings from MRF and Hp. The recordings from frontal cortex show increase of share of frequencies 10-13 cps. Ethanol increases the share of low frequencies in EEG recordings and decreases the share of fast frequencies. Mianserin increases its influence on fast frequencies.
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PMID:Influence of mianserin on some central effects of ethanol. 1220 20

Ethanol concentrations were measured in femoral venous blood in deaths attributed to acute alcohol poisoning (N = 693) or chronic alcoholism (N = 825), according to the forensic pathology report. Among acute alcohol poisonings were 529 men (76%) with mean age 53 years and 164 women (24%) with mean age 53 years. In the chronic alcoholism deaths were 705 men (85%) with mean age 55 years and 120 women (15%) with mean age 57 years. The blood-ethanol concentrations were not related to the person's age (r = -0.17 in acute poisonings and r = -0.09 in chronic alcoholism). The distribution of blood-ethanol concentrations in acute poisoning cases agreed with a normal or Gaussian curve with mean, median, standard deviation, coefficient of variation, and spread of 0.36 g/100 mL, 0.36 g/100 mL, 0.086 g/100 mL, 24% and 0.074 to 0.68 g/100 mL, respectively. The corresponding concentrations of ethanol in chronic alcoholism deaths were not normally distributed and showed a mode between 0.01 and 0.05 g/100 mL and mean, median, and spread of 0.172 g/100 mL, 0.150 g/100 mL, and 0.01 to 0.56 g/100 mL, respectively. The 5th and 95th percentiles for blood-ethanol concentration in acute poisoning deaths were 0.22 and 0.50 g/100 mL, respectively. However, these values are probably conservative estimates of the highest blood-ethanol concentrations before death owing to metabolism of ethanol until the time of death. In 98 chronic alcoholism deaths (12%) there was an elevated concentration of acetone in the blood (>0.01 g/100 mL), and 50 of these (6%) also had elevated isopropanol (>0.01 g/100 mL). This compares with 28 cases (4%) with elevated blood-acetone in the acute poisoning deaths and 22 (3%) with elevated blood-isopropanol. We offer various explanations for the differences in blood-ethanol and blood-acetone in acute poisoning and alcoholism deaths such as chronic tolerance, alcohol-related organ and tissue damage (cirrhosis, pancreatitis), positional asphyxia or suffocation by inhalation of vomit, exposure to cold coupled with alcohol-induced hypothermia, as well as various metabolic disturbances such as hypoglycemia and ketoacidosis.
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PMID:Comparison of blood-ethanol concentration in deaths attributed to acute alcohol poisoning and chronic alcoholism. 1287 10

Ethyl alcohol (ethanol) is readily absorbed from all parts of the gastrointestinal tract due to its hydrophilic potential. The biological effects in humans refer to practically every organ and system. The basic enzyme involved in its oxidation is alcohol dehydrogenase. Another important metabolic pathway is the Microsomal Ethanol-Oxidizing System (MEOS). Toxic effect on basic cell functions is produced both by ethanol and acetic aldehyde, its oxidation product which accounts for most of the acute and delayed effects of ethanol toxicity. In acute ethanol intoxication's the CNS symptoms are the first to manifest. Ethanol affects the CNS functions mainly through stimulating opiate and benzodiazepine receptors and a number of neurotransmitters. However, the attempts to diminish the toxic effects of ethanol on CNS by blocking the affected receptors have proved to be ineffective. In acute poisoning a basic essential is to sustain vital functions by following the principles of intensive care. Each case of acute ethanol intoxication must be subject to neurological examination for possible cerebro-cranial traumas. The diagnostics and treatment procedures should take account of the possible symptoms: convulsions, respiratory and cardiac failure, hypoglycemia, hypothermia, and severe gastric dysfunction. Vital signs monitoring and control of acid-base and water-electrolyte balance are a must. The toxic properties of ethanol metabolites can be particularly hazardous to patients treated with disulfiram. The patients who develop "antabuse response" should be given immediately iron and vitamin C intravenously.
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PMID:[Biological and toxic effects of ethanol: diagnostics and treatment of acute poisonings]. 1456 85

The Edinger-Westphal nucleus (EW) is a brain region that has recently been implicated as an important novel neural target for ethanol. Thus, the EW is the only brain region consistently showing elevated c-Fos expression following both voluntary and involuntary ethanol administration. Ethanol-induced c-Fos expression in the EW has been shown to occur in urocortin I-positive neurons. Moreover, previous reports using several genetic models have demonstrated that differences in the EW urocortin I system are correlated with ethanol-mediated behaviours such as ethanol-induced hypothermia and ethanol consumption. The aim of this study was to confirm these relationships using a more direct strategy. Thus, ethanol responses were measured following electrolytic lesions of the EW in male C57BL/6J mice. Both EW-lesioned and sham-operated animals were tested for several ethanol sensitivity measures and ethanol consumption in a two-bottle choice test. The results show that lesions of the EW significantly disrupted ethanol-induced hypothermia, while having no effect on pupillary dilation, locomotor activity or ethanol-induced sedation. In addition, EW-lesioned animals showed significantly lower ethanol preference and total ethanol dose consumed in the two-bottle choice test. EW-lesioned animals also consumed less sucrose than sham-operated animals, but did not have altered preferences for sucrose or quinine in a two-bottle choice test. These data support previously observed genetic correlations between EW urocortin I expression and both ethanol-induced hypothermia and ethanol consumption. Taken together, the findings suggest that the EW may function as a sensor for ethanol, which can influence ethanol consumption and preference.
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PMID:Lesions of the Edinger-Westphal nucleus in C57BL/6J mice disrupt ethanol-induced hypothermia and ethanol consumption. 1535 28

Using pituitary adenylate cyclase-activating polypeptide (PACAP)-deficient mice, we investigated whether PACAP is involved in the intoxicating effects of ethanol. The structure of PACAP is highly conserved during evolution, and in Drosophila, loss-of-function mutations in a PACAP-like neuropeptide gene, amnesiac, result in impairment of memory retention and increased sensitivity to ethanol. In mice, PACAP deficiency is associated with impaired memory performance and hippocampal long-term potentiation (LTP), however, sensitivity to ethanol has not been well investigated. Here, we addressed this issue in our recently developed PACAP-deficient mice. Sleep time (duration of the loss of righting reflex) was markedly shortened in PACAP-deficient mice compared with wild-type, although latency to the loss of righting reflex was not different between the two groups. Ethanol-induced hypothermia in wild-type control mice was significantly reduced in PACAP-deficient mice. Blood ethanol levels were not different between the two groups, excluding the possibility of increased ethanol metabolism. Thus, in contrast to that in Drosophila, PACAP deficiency in mammals caused a reduced sensitivity to ethanol. However, in both cases, PACAP or amnesiac products are likely to play significant roles in modifying the intoxicating effects of ethanol.
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PMID:Reduced hypothermic and hypnotic responses to ethanol in PACAP-deficient mice. 1551 98

The process of cooling is always associated with the depletion of energetic reserves and burning the ketone bodies covers the tissues' needs. Ethanol shows antiketonaemic effects changing the cellular redox potential, inhibiting beta-oxidation of fatty acids, stimulating the release of insulin and inhibiting the release of its antagonist. The aim of the study was to determine whether the cooling process of the organism in the presence of ethanol intoxication may be related to inhibition of the physiological mechanism of ketogenesis induced by hypothermia. The study involved the 67 autopsy cases from 1996 to 2002, in which the circumstances of death indicated the effects of overcooling. This was confirmed on the basis of the data from the Prosecutor's Offices. Then, the chromatograms of autopsy blood alcohol determinations were analyzed and the acetone levels recorded. The analysis supported the hypothesis that the severity of ketosis is inversely proportional to the blood ethanol concentration. Furthermore, it demonstrated that signs of prolonged cold exposure were less frequently observed in unsober persons (frostbites, gastric hemorrhages). Increased sensitivity of intoxicated individuals to cold may be related not only to the dilation of the peripheral vessels, inhibition of shivering thermogenesis caused by muscle relaxation, central nervous system depression and behavioral factors but also to the antiketonaemic effects of ethanol.
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PMID:Biochemical background of ethanol-induced cold susceptibility. 1555 11


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