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

The effects of certain experimental variables on rodents brain and liver alcohol--(ADH) and aldehyde-dehydrogenase (LALDH) were evaluated. The in vivo and in vitro effect of chlorpromazine on these enzymes was determined. Short-term housing under complete darkness differentially inhibited ADH and ALDH in distinct brain regions with ADH showing more sensitivity than ALDH. The hepatic enzymes studied were not affected by such housing conditions but a non-competitive inhibition of L-ALDH occurred as a consequence of exposure to UV lighting for 3 consecutive weeks. Short-term treatment with chlorpromazine inhibited striatal ADH which was not affected by experimentally-induced hypothermia. Likewise, both hepatic and testicular ADH were noncompetitively inhibited in vitro by chlorpromazine. The results suggest sensitivity of brain and hepatic ADH to environmental housing conditions and indicate a similarity between peripheral and cerebral ADH responses to chlorpromazine. The modulation of ADH and/or ALDH may facilitate the formation of endogenous biogenic amines derived alkaloids which have been implicated in alcohol and extrapyramidal side effects.
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PMID:Cerebral and peripheral neurotoxicity of chlorpromazine and ethanol interaction: implications for alcohol and aldehyde dehydrogenase. 174 39

To examine the interactive effects of ethanol (EtOH) and ambient temperature, 10-, 16-, and 20-day-old rat pups ingested pairings of sucrose solution and various doses of ethanol (intubated intragastrically) and were then exposed to relatively low or relatively high ambient temperatures. Ten- and 20-day-old pups required a higher EtOH dose than did 16-day old pups for conditioning of a sucrose aversion and for hypothermia. These age-related differences might be due to ontogenetic changes in the production and accumulation of acetaldehyde, a metabolite of EtOH. For all ages, EtOH-induced hypothermia was necessary for conditioning of the taste aversion, which is in accord with results of previous tests with adult rats (Cunningham, Hawks, & Niehus, 1988).
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PMID:An ontogenetic comparison of ethanol-mediated taste aversion learning and ethanol-induced hypothermia in preweanling rats. 177 9

It has been proposed that ethanol can be oxidized in brain via the peroxidatic activity of catalase and that centrally formed acetaldehyde may mediate several of the psychopharmacological actions of ethanol. The present study was designed to investigate the role of brain catalase in the mediation of ethanol-induced narcosis, hypothermia and lethality in rats. Rats were pretreated with the catalase inhibitor 3-amino-1,2,4-triazole (AT) or saline. Five hours later, animals in each pretreatment group received IP injections of ethanol (3 or 4 g/kg). Ethanol-induced narcosis was significantly attenuated in AT-pretreated rats compared to the saline control group. As well, AT pretreatments reduced significantly the lethal effect of these ethanol doses. However, AT-pretreated ethanol-injected animals significantly reduce their body temperature as compared to the saline-ethanol animals. Blood ethanol determinations revealed that AT did interfere with ethanol metabolism. AT inhibits significantly brain catalase activity at all doses used in this study. The results indicate a role for brain catalase in ethanol effects. Furthermore, they suggest that catalase may be involved in the oxidation of ethanol in brain and that centrally formed acetaldehyde may play a role in ethanol-induced narcosis and lethality, but not hypothermia.
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PMID:Effect of 3-amino-1,2,4-triazole on ethanol-induced narcosis, lethality and hypothermia in rats. 192 13

Calcium pantothenate (CaP), calcium 4'-phosphopantothenate (CaPP), pantethine, panthenol, sulfopantetheine and CoA decrease acute toxicity of acetaldehyde in mice. All studied compounds diminish duration of the narcotic action of ethanol--ET (3.5 g/kg intraperitoneally) in mice and rats. In the latter this effect is realized at the expense of "long sleeping" and "middle sleeping" animals. CaP (150 mg/kg subcutaneously) and CaPP (100 mg/kg subcutaneously) prevent hypothermia and a decrease of oxygen consumption in rats induced by ET administration. Combined administration of ET, CaP and CaPP leads to a characteristic increase of acid-soluble CoA fractions in the rat liver and a relative decrease of acetyl CoA synthetase and N-acetyltransferase reactions. The antitoxic effect of preparations of pantothenic acid is not mediated by CoA-dependent reactions of detoxication, but most probably is due to intensification of ET oxidation and perhaps to its elimination from the organism.
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PMID:[The protective effect of pantothenic acid derivatives and changes in the system of acetyl CoA metabolism in acute ethanol poisoning]. 290 77

Studies were carried out to determine whether the disulfiram-ethanol reaction (DER) in the rat could be correlated with blood acetaldehyde, ethanol, and liver aldehyde dehydrogenase (ALDH) inhibition. Both hypothermia and hypotension were used as indices of the DER. Female Sprague-Dawley rats were given disulfiram (DSF) (100 mg/kg, i.p.) and low and high liver ALDH determined. No effect on high Km ALDH was found. Inhibition of low Km ALDH was dependent on DSF pretreatment time, with significant inhibition observed at 6, 8, and 12 hr following DSF. In rats receiving ethanol only, maximal blood ethanol was reached within 120 min. Blood acetaldehyde was almost undetectable. No change in rat core temperature was observed. In rats pretreated with DSF (100 mg/kg, i.p.) 8 hr before ethanol challenge (1 g/kg, i.p.), a marked increase in blood acetaldehyde was found and remained elevated throughout the temperature and blood pressure monitoring period. Blood ethanol reached a maximum within 90 min and then declined. Maximal hypothermia and hypotension occurred 120 min after ethanol. The administration of the dopamine receptor blocker pimozide (0.5 mg/kg, i.p.) 60 min before ethanol challenge, attenuated the hypothermia and hypotension. Pimozide was effective when given either 60 min before ethanol or 30 min after ethanol. The onset and duration of hypothermia and hypotension during the DER appears to follow the rise and fall of blood ethanol but not blood acetaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disulfiram-ethanol reaction in the rat. 1. Blood alcohol, acetaldehyde, and liver aldehyde dehydrogenase relationships. 351 91

SAL is a tetraisoquinolein (T.I.Q.), resulting from the condensation of acetaldehyde and dopamine. SAL, injected intraperitoneally, is active in tests commonly used to screen potential antidepressants. This effect is especially studied by using antagonism of apomorphine, reserpine, oxotremorine-induced hypothermia. The noradrenergic system seems to be involved in the mechanism of action.
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PMID:Psychopharmacological profile of salsolinol. 380 19

Adult guinea-pigs were treated with ethanol (2.5 g/kg, IP) or acetaldehyde (100 mg/kg, IP) and exposed to moderate cold (+4 degrees C) for 50 minutes. Controls were given 0.9% NaCl solution. The hypothalamic catecholamines norepinephrine (NE) and dopamine (DA) and also norepinephrine and epinephrine (E) in the serum were analyzed by high-performance liquid chromatography with an electrochemical detector. Blood glucose, free fatty acids and glycogen in the liver and skeletal muscle were also measured. Acetaldehyde caused a similar drop in colon temperature as did ethanol, but neither could prevent cold-induced vasoconstriction in the ear lobe. Ethanol significantly reduced the concentration of NE in the hypothalamus compared to the controls. Acetaldehyde had a tendency to lower hypothalamic NE. There was no significant difference between drug-treated groups in NE concentration. Neither ethanol nor acetaldehyde had any effect on hypothalamic DA. In the ethanol group serum E and glucose were significantly elevated compared to the acetaldehyde group. Serum glucose was also higher compared to the controls, and the difference in serum E concentration near the level of significance. No significant differences were found between the groups in serum NE, FFA or skeletal muscle and liver glycogen concentration. The results point to a possible central effect of ethanol during a short-term moderate cold exposure. The effects of acetaldehyde on neuronal tissue remain speculative, but a possible effect on noradrenergic neurons cannot be ruled out. Although the hypothermic effect of acetaldehyde corresponded that of ethanol, further experiments are required to elucidate the role of acetaldehyde in ethanol-induced hypothermia.
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PMID:Hypothalamic and serum catecholamines in ethanol and acetaldehyde treated guinea-pigs. Relation to moderate short-term cold exposure. 381 45

The effects of intracerebral injection of salsolinol, the condensation product of dopamine and acetaldehyde, were compared in LS and SS mice selectively bred for differential sleep time following an intraperitoneal injection of ethanol. Salsolinol differentially affected open-field activity in the two mouse lines. Low doses of salsolinol increased open-field activity in the SS line; no such effects were obtained in the LS line. Larger doses decreased activity in both lines but the LS mice were more sensitive to this effect. Similar effects on open-field activity have been reported for ethanol in these same lines of mice. A 40 micrograms dose of salsolinol increased ethanol-induced sleep time in both lines but the increase was greater in the LS line. With lower doses of salsolinol the duration of ethanol-induced sleep time decreased in SS mice and increased in LS mice. This effect of salsolinol on sleep time most likely involves some CNS mechanism since salsolinol did not alter ethanol elimination rate in the two lines of mice. A more severe and prolonged hypothermia developed in LS mice following injections of salsolinol or equal doses of ethanol; however, equi-hypnotic doses of ethanol elicited similar hypothermic responses. Taken together, these data support a possible role for salsolinol in ethanol's actions.
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PMID:Behavioral effects of ethanol and salsolinol in mice selectively bred for acute sensitivity to ethanol. 671 55

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

Aldehyde dehydrogenase 2 (ALDH2) is an important enzyme that oxidizes acetaldehyde. Approximately 45% of Chinese and Japanese individuals are inactive ALDH2 phenotype; acute acetaldehyde toxicity has not been evaluated in these populations. We compared the acute acetaldehyde toxicity between wild-type (Aldh2+/+) and Aldh2-inactive transgenic (Aldh2-/-) mice who were administered an intraperitoneal (ip) injection of a single dose of acetaldehyde. This comparison was made based on the LD(50) values of acetaldehyde and the symptoms following the ip injection. Blood acetaldehyde level was measured in the 400 mg/kg dose group. Immediately after administration of acetaldehyde, the mice exhibited hypoactivity and staggering gait. Subsequently, symptoms such as pale skin, prone position, coma, and abnormal deep respiration were observed. In cases of death, dyspnea, wheezing, and hypothermia were observed from 15 to 30 min after the administration. In cases of survival, crouching, bradypnea, flushing and piloerection were observed. Significant latency of symptom recovery was found in the Aldh2+/- mice as compared with the Aldh2+/+ mice; however, no statistical difference was observed in the acetaldehyde LD(50) values. This might be attributable to the absence of a significant difference in the blood acetaldehyde concentrations in both mice during the first 0-15 min following administration; however, acetaldehyde elimination delay was observed in the Aldh2-/- mice as compared with the Aldh2+/+ mice. Acetaldehyde toxicity difference was observed between the Aldh2+/+ and Aldh2-/- mice; however, no difference in acetaldehyde lethality was observed by administration of a single dose of an ip acetaldehyde injection.
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PMID:Aldehyde dehydrogenase 2 activity affects symptoms produced by an intraperitoneal acetaldehyde injection, but not acetaldehyde lethality. 1640 40


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