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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol aggravates benzodiazepine-induced central nervous depression by pharmacokinetic and/or pharmacodynamic interactions and Ro 15-1788 reverses promptly the hypnotic effects of benzodiazepines. We therefore studied the acute effects of Ro 15-1788 on the ethanol-induced sedation in six healthy male subjects. Subsequently to an oral loading dose (0.54 g ethanol kg-1) ethanol was infused for 4 h (0.15 g ethanol kg-1 h-1) and steady state blood levels between 0.9 to 1.2 g l-1 were reached within 2 h. At steady state and during the elimination phase of ethanol an intravenous bolus of 0.5 mg Ro 15-1788 or placebo was administered in a randomized, double-blind crossover fashion. The marked sedative effects of ethanol as assessed by visual analogue scales (2 to 6 fold increase in the sedation index), and choice reaction time (25 to 40% prolongation) were not affected by Ro 15-1788. However, the pharmaco-EEG indicated that Ro 15-1788 seems to reverse transiently the ethanol-induced changes in total alpha, delta, and slow alpha bands. There was no pharmacokinetic interaction between both agents since elimination of Ro 15-1788 (t1/2 = 1.2 +/- 0.7 h) and of ethanol (0.17 +/- 0.02 g l-1 h-1) were in good agreement with control values. Thus, it could be concluded that Ro 15-1788 might affect for a short while the action of ethanol by interfering with the benzodiazepine receptors.
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PMID:Does the benzodiazepine antagonist Ro 15-1788 antagonize the action of ethanol? 309 70

This study deals with the interaction between high pressure and a sub-hypnotic dose of ethanol in rats. Male Sprague-Dawley rats were given either ethanol 1.5 g/kg or saline IP and subsequently exposed to 1 atmosphere absolute pressure (ATA) air or to 1, 12, 24 or 48 ATA of helium-oxygen (heliox). The gas temperature was adjusted to offset ethanol and helium-induced hypothermia. Ethanol induced a characteristic unsteady pattern of locomotion which was completely reversed at 48 ATA, partially reversed at 24 ATA, but not affected at 12 ATA. Other behavioral effects of ethanol such as depression of total motor activity and rearing were similarly affected. Blood and brain concentrations of ethanol in the pressure groups did not differ significantly from concentrations measured in the 1 ATA groups. A similar pattern of reversal was observed whether the compression was initiated 4, 10 or 16 min after injection. These results show that hyperbaric exposure antagonizes the depressant effect of ethanol on spontaneous behavior in rats. This antagonism does not appear to be due to changes in ethanol distribution or elimination.
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PMID:Pressure reversal of the depressant effect of ethanol on spontaneous behavior in rats. 335 18

The effect of ethanol on behavioral thermoregulation in the goldfish, Carassius auratus, was studied by adding ethanol to a horizontal aquatic temperature gradient which allowed each fish to select its preferred temperature within a range of about 9 degrees C to 33 degrees C. Alternating exposure to 1.0% (v/v) ethanol and water showed that fish (10 to 15 g) responded to ethanol by selecting lower temperatures. Onset and disappearance of the effect occurred within 10 min of exposure to or removal from ethanol. Fish exposed to 1.0% ethanol for 3 hr did not show acute tolerance. When fish were exposed to increasing concentrations of ethanol from 0.0% to 1.7%, the lowest concentration to elicit a response was 0.5% ethanol. The magnitude of the response plateaued at 0.7% ethanol. At this concentration and above, selected temperatures remained about 2 degrees C below temperatures selected by controls. Because thermoregulatory responses of fish are behavioral and relatively easy to observe and quantify, goldfish offer a useful model for the study of ethanol effects on central nervous system control of thermoregulation. Ethanol produces a prompt, stable, and reproducible depression of selected temperature by lowering the thermoregulatory set point in the goldfish.
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PMID:The effect of ethanol on temperature selection in the goldfish, Carassius auratus. 336 19

Ethanol in vitro inhibited synaptosomal sodium-dependent, high-affinity choline uptake, the rate-limiting step in the synthesis of acetylcholine. This inhibition occurred with ethanol concentrations as low as 50 mM, was reversible and was not attributable to ethanol effects on synaptosomal membrane potential. In contrast, ethanol concentrations as high as 400 mM had no effect on synaptosomal high-affinity uptake of gamma-aminobutyric acid, a major inhibitory neurotransmitter in the central nervous system. The observed ethanol inhibition of choline uptake is consistent with suggestions that depression of cholinergic systems is important in acute ethanol intoxication.
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PMID:Ethanol inhibition of synaptosomal high-affinity choline uptake. 341 25

Ethanol causes depression of cardiac function. A new model in hamsters was developed for studying ethanol-induced myocardial dysfunction and the effects of verapamil in preventing the functional and metabolic derangements caused by ethanol ingestion were evaluated. Ethanol was added to the drinking water of hamsters in increasing amounts, reaching 50% from 5 weeks on. A control group received plain water only. A third group had verapamil (1.75 mg/cc) added to the ethanol-water mixture to evaluate its potential protective effect. After 5, 7 and 12 weeks, the animals were killed and the hearts perfused using a Langendorff heart preparation. Pressures were recorded and metabolic analysis was performed by the freeze-clamp technique. Compared with control hearts, the hearts from hamsters ingesting ethanol showed significant depression of developed pressure and maximal rate of rise in pressure. There was also significant depression of high energy phosphates and adenosine. The animals drinking the ethanol-verapamil mixture had preservation of left ventricular performance and high energy phosphates, with measurements indistinguishable from those of the control group. In summary, verapamil prevented the development of myocardial depression and preserved normal energy metabolism in hearts of hamsters drinking 50% ethanol.
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PMID:Verapamil prevents the development of alcoholic dysfunction in hamster myocardium. 358 21

Ethanol elimination from the blood of rats with different psychophysiological features was studied using gas chromatographic head-space analysis in the general complex of tests aimed at determination of ethanol consumption. The selection of animals with different levels of the initial alcohol motivation was performed according to modified Porsolt's method. It was shown that the initial level of predisposition to depression-like states is in a dose-dependent correlation with the high rate of ethanol elimination. This is suggested to be one of the genetic indications which promotes the formation of the initial alcohol motivation and the development of experimental alcoholism.
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PMID:[Correlation between the rate of ethanol elimination and the psychophysiological characteristics of rats]. 359 32

In male Swiss-Webster mice sleep time (hypnosis) was used as an index of ethanol-induced central nervous system depression. Ethanol (4 g/kg, IP) was administered to animals and the onset to sleep time (loss of the righting reflex) and the duration of sleep time were recorded. At the end of the ethanol-induced sleep time, taurine (7.5, 15 or 25 mumol/kg, ICV) was injected. Immediately after the ICV injection of taurine the mice again lost the righting reflex. This effect of taurine occurred in a dose-dependent fashion. In the absence of ethanol, taurine (25 mumol/kg, ICV) did not produce a significant sleep time. In another experiment when TAG, 6-amino-methyl-3-4H-1,3,4-benzothiadiazine-1,1-dioxide HCl, (a taurine antagonist) was given to mice, TAG (0.9 mumol/kg, ICV) significantly reduced the effect of taurine (7.5, 15 and 25 mumol/kg, ICV) to reinstate a sleep time in the presence of ethanol. TAG, however, did not alter ethanol-induced sleep time. These results indicate that taurine (ICV) can enhance the central depressant action of ethanol and that this effect of taurine can be attenuated by TAG. The antagonism of taurine by TAG appears to be noncompetitive in nature.
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PMID:Ethanol-induced sleep time: interaction with taurine and a taurine antagonist. 362 38

This study examined the effects of ethanol and hereditary cardiomyopathy on sodium and water excretion by golden Syrian hamsters of both sexes. Ethanol (4 g/kg) or the isotonic saline vehicle were injected IP into 60-70-day-old hamsters of normal and cardiomyopathic (BIO 14.6) strains. Urine and blood were collected after 90 or 350 min in different groups. Cardiomyopathic hamsters more quickly lost their righting responses, eliminated ethanol more slowly, and had lower urine volume and sodium excretion than normal hamsters after ethanol injections. Plasma creatine kinase levels were normal in all animals tested, indicating no active skeletal or cardiac lesioning in the cardiomyopathic hamsters at the time of the experiment. Some factors which could contribute to the increased CNS and renal sensitivity to ethanol in cardiomyopathic hamsters include impaired ethanol metabolism, enhanced myocardial depression, and reduced atrial content of natriuretic peptides. The results do not owe to decompensated heart failure. Thus, the genetic mutation which causes skeletal and cardiac myopathy in these hamsters may also affect the metabolism and sensitivity to ethanol.
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PMID:Ethanol in cardiomyopathic hamsters: Na and water excretion and righting response. 371 87

Effects of experimental exposure to toluene (3.2 mmol/m3, ie, 300 mg/m3) for 4.5 h and ethanol ingestion (15 mmol/kg) on the results of four performance tests, symptoms, mood, and physiological indices of wakefulness were studied in 12 male volunteers. Toluene exposure produced symptoms like headache and local irritation, as well as a weak depression of heart rate during rest, but did not reduce performance capability. Ethanol ingestion impaired performance on two of the tests and also increased heart rate. Mood was likewise altered by ethanol, but no increase in subjective symptoms due to ethanol ingestion could be demonstrated. Physiological indices of wakefulness were not affected by toluene exposure or by ethanol intake. No interaction effects were found.
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PMID:Experimental exposure to toluene in combination with ethanol intake. Psychophysiological functions. 372 94

The effect of ethanol and other aliphatic alcohols on the intestinal transport of 5-methyltetrahydrofolate and folic acid was examined using everted sacs from rat jejunum. Ethanol added to the mucosal medium inhibited the transport of both folate compounds in a parallel manner, and the inhibition increased with increasing ethanol concentration (0.5-10% v/v). Ethanol at 3% v/v in the mucosal medium caused: depression in the pH dependency of the active transport of 5-methyltetrahydrofolate; higher inhibition in the transport of low concentration (0.1 microM) than high concentration (10 microM) of 5-methyltetrahydrofolate, and inhibition in the active accumulation against a concentration gradient of 5-methyltetrahydrofolate and L-leucine. Methanol, propanol and butanol also inhibited the transport of the folate compounds; and in general, the inhibitory effect increased with the increase in the number of carbon atoms in the hydrophobic chain. This study indicates that ethanol and other alcohols inhibit the intestinal transport of folates, that the degree of inhibition is related to the concentration and chain length of the alcohol, that the inhibition is not specific for folates and finally that the mechanism of inhibition is multifactorial.
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PMID:Effect of ethanol and other aliphatic alcohols on the intestinal transport of folates. 378 Nov 8


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