Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physical dependence upon ehtanol induced in rats is in several respects similar to the tremulous and convulsive components of the ethanol withdrawal syndrome observed in man. These include short duration of the induction period, pattern of continuous ethanol consumption, rectilinear clearance of blood ethanol during prodromal detoxication phase and the onset of the ethanol dependence phase at relatively high blood ethanol concentrations. During the ethanol withdrawal period two phases are distinguished in both species: (1) Prodromal detoxication phase characterized by a spectrum of signs and responses of ethanol intoxication. (2) Ethanol dependence phase characterized by a spectrum of withdrawal signs and reactions. The successive onset and disappearance of the two sets of signs and reactions during both phases of the ethanol withdrawal period constitute a continuum of effects and responses and represent a reversal in the CNS function from the extremes of ethanol depression to the extremes of hyperexcitability.
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PMID:Comparison of ethanol withdrawal syndrome in humans and rats. 59 77

Glucose and water transport is depressed in the hamster jejunum in vivo by ethanol (4.8%) which also produced fluid-filled blebs at the tips of the villi. The epithelial cells over the blebs appeared stretched and cuboidal, the lateral intercellular spaces (LIS) were no longer recognizable, and the lacteals were closed. Forty-five minutes after discontinuation of the ethanol, water transport returned to normal while glucose transport remained depressed. At this time the villus structure had returned to normal. The blebs had disappeared, the LIS were again recognizable, and their appearance and number were similar to those in the control animals. Thus, the depression of water transport correlated with the obvious structural changes caused by ethanol; however, the depression of glucose absorption is associated with some effect of ethanol not evident by routine light microscopy.
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PMID:The correlation of ethanol-induced depression of glucose and water transport with morphological changes in the hamster jejunum in vivo. 63 49

The ventilatory responses mediated by the central and peripheral chemoreceptors were separately assessed in eight healthy volunteers before and after the oral ingestion of ethanol in a dose of 0.75 ml/kg. No significant depression of the central response was observed, but a significant depression of the peripheral response was observed at 25 and 95 minutes after the consumption of ethanol. The peripheral chemoreceptor stimulus was the simultaneous increase of hypoxia and hypercapnia and this novel method is described.
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PMID:The effect of ethanol on the ventilatory responses mediated by the peripheral chemoreceptors in man. 65 90

Rats fed a special liquid fat diet had a higher level of liver triglycerides than rats fed a normal solid chow diet. The ingestion of ethanol induces a concomitant increase in hepatic triglycerides and a depression of ATP levels. Pure adenine base administered orally produces a significant reduction of hepatic triglycerdies and partially restores ATP levels in the chronic ethanol treated rat. Comparable doses of oral ATP are not effective. Pure guanine base and GTP failed to inhibit the ethanol-induced fatty liver and ATP depression.
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PMID:The effect of purine bases and nucleotides on ethanol-induced fatty liver syndrome. 67 63

Ethanol (1 g/kg, iv) produced a peak depression of acetylcholine release from the cat sensorimotor cortices within 30 min of the ethanol administration but recovery to control levels occurred in the following 30 min. However, the concentrations of ethanol in the blood and in the solution bathing the cortex remained stable during this recovery period. This example of acute tolerance to ethanol is possibly related to the well-known acute tolerance that develops to the behavioural effects of ethanol.
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PMID:Acute tolerance to ethanol on the release of acetylcholine from the cat cerebral cortex. 68 92

The definition of abuse and dependence of non-narcotic analgesics should take into consideration the interaction of drug and personality. Usually, definitions are based on qualitative aspects of the risk-benefit ratio in the use of psychotropic drugs. By means of modern research methods in epidemiology and clinical psychology, quantitative aspects might be integrated in the process of defining persons and drugs when evaluating their risk of abuse or dependence. In a prospective field study with working housewives of northwestern Switzerland who showed objective evidence of intake of non-narcotic analgesics and a control group, the interaction of drug use and personality features has been investigated. There was significant evidence that heavy use of non-narcotic analgesics was paralleled with a high risk of depression, emotional liability and disturbance in sexual identity. Using urine analysis, the study group was divided into two subgroups showing low or high intake of drugs, respectively. Special attention was focused on persons shifting from the study group into the control group and vice versa.
Drug Alcohol Depend 1978 Nov
PMID:Use and abuse of non-narcotic analgesics. 72 Feb 12

The antidiarrheal drugs loperamide and diphenoxylate were tested for their ability to potentiate central nervous system depression induced by ethanol in mice and nethohexital in rats. Oral diphenoxylate potentiated the loss of righting reflex (hypnosis) at 10 mg/kg in mice and at 5 mg/kg in rats, doses which were considerably lower than those required to induce morphine-like behavior in mice and rats. Oral loperamide did not potentiate hypnosis. Increased incidence and duration of hypnosis was observed with loperamide only at very high, nearly toxic doses (100 mg/kg in mice and 80 mg/kg in rats) and these doses induced only nonspecific central nervous system depression. The failure of loperamide to potentiate the action of hypnotics confirms data from clinical trials which showed that loperamide is essentially free of central depressant effects when given orally.
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PMID:Interaction of loperamide and diphenoxylate with ethanol and methohexital. 74 64

Pretreatment of mice with either ethanol, pentobarbital or morphine protected against the lethal effects of hemicholinium-3 (HC-3) but not curare. The protective action of these compounds was not due to an induced release of corticosteroids in vivo since administration of prednisolone did not protect against HC-3 toxicity. The protective action of morphine was reversed by Nalline hydrochloride. The results suggest that the site of the protective action of ethanol, pentobarbital and morphine and the site of action of the lethal respiratory depression by HC-3 are central in origin.
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PMID:Effect of ethanol, pentobarbital and morphine on the toxicity of hemicholinium-3 and d-tubocurarine in mice. 74 65

We evaluated the effect of ethanol on exercise performance until angina in 12 patients in a double-blind, randomized study. The mean resting heart rate times systolic blood pressure was not changed after Fresca but was increased after 2 ounces of ethanol (P less than 0.001) and after 5 ounces of ethanol (P less than 0.01). Compared to the control periods, the mean exercise time until angina was not different after Fresca but was decreased after 2 ounces of ethanol (P less than 0.001) and after 5 ounces of ethanol (P less than 0.001). Compared to the control periods, the mean maximal ischemic ST-segment depression after angina was not changed after Fresca but was increased after 2 ounces of ethanol (P less than 0.01) and after 5 ounces of ethanol (P less than 0.001). Drinking 5 ounces or 2 ounces of ethanol decreases exercise duration until angina and increases ischemic ST-segment depression after angina.
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PMID:Effect of ethanol on angina pectoris. 77 61

Low concentrations of several emetic, purgative or irritant drugs in the absence of added co-factors stimulated conversion of arachidonic acid to prostaglandin E2 and F2alpha by prostaglandin synthetase extracted from bull seminal vesicles (BSV prostaglandin synthetase). Their effect was dependent on concentration and time. Stimulation of BSV prostaglandin synthetase by apomorphine, aloes, tyramine or zingerone was increased several-fold by addition of reduced glutathione to the incubation medium, whereas hydroquinone, a phenolic co-factor of prostaglandin synthetase caused slight depression. From this finding and from the observation that many of the stimulant drugs possess a phenolic group, whereas their inactive relatives lack such a group, it is suggested that these stimulant drugs act as co-factors for prostaglandin synthetase in place of hydroquinone. Aloes, tyramine, ethanol and quipazine also produced a dose-related increase in resting tone of the isolated fundus of the rat stomach. This increase occurred at concentrations comparable to those effective in stimulating BSV prostaglandin synthetase, and was abolished by acetylsalicylate. These findings support the view that certain drugs exert some of their pharmacological effects by stimulating prostaglandin synthetase.
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PMID:Stimulation of prostaglandin biosynthesis by drugs: effects in vitro of some drugs affecting gut function. 82


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