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)

Acute ethanol influence on field L auditory evoked potentials (AEP) was studied in 4-8-days-old altricial nestlings of pied flycatcher. Nestlings were presented with tone pips related with the realization of natural behaviour (2.0 and 5.0 kHz) and bearing no meaning for the behaviour of the young of the age under study (3.0 kHz). Ethanol ingestion was found to reduce the maturity index (MI) of AEP in response to "behavioural" but not to control frequencies; this effect was first observed at day 5, when nestlings eyes opened and defence behaviour appeared, while previously formed feeding behaviour was significantly modified. During the next 2 days alcohol had a greater effect upon the AEP in response to 2.0 kHz tone pips, related with feeding behaviour of increasing complexity than upon the AEP in response to 5.0 kHz, related with the defence behaviour that remained relatively constant. The previous data concerning the effect of alcohol on unit activity are used to support the view that MI increase during the early postembryonic ontogeny is due to the involvement of neurons with newly formed behavioural specializations into the subserving of new behavioural patterns while the decrease of MI under alcohol is due to the depression of activity in these neurons.
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PMID:[The effect of acute alcohol administration on auditory evoked potentials in altricial nestlings during the development of natural behavior]. 133

The effects of acute ethanol administration on acid-base balance and hemodynamic parameters were studied in a canine model. Ten mongrel dogs, anesthetized and maintained on a volume ventilator, underwent splenic artery ligation 30 minutes prior to study. Group A (N = 5) served as controls. Thirty minutes after drug administration, the animals underwent a 20-cc/kg hemorrhage over 15 minutes. Thirty minutes postphlebotomy, resuscitation was performed with the same volume of homologous blood. Acid-base and hemodynamic parameters were monitored over 3.5 hours. Ethanol levels peaked 60 minutes following administration at 207 +/- 13 mg%. During the entire study, no differences were observed in heart rate, pulmonary capillary wedge pressure, systemic vascular resistance index, pO2, or pCO2, between the two groups. Following hemorrhage, statistically significant decreases in pH, mean arterial pressure (MAP), cardiac index (CI), and left ventricular stroke work index (LVSWI) developed in group A compared to controls. Maximal disparity developed in pH (7.21 +/- 0.05 to 7.33 +/- 0.02, P < 0.01), MAP (67 +/- 11 v 110 +/- 9 torr, P < 0.01), CI (1.69 +/- 0.24 compared to 2.72 +/- 0.19 L/min/M2, and LVSWI (18.7 +/- 1.2 compared to 44.9 +/- 4.8 gr-meter/M2/beat, P < 0.01) at 60, 45, 30, and 75 minutes postphlebotomy. In this study, ethanol directly or indirectly caused an increased metabolic acidosis and myocardial depression in the post-hemorrhage period.
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PMID:Protracted metabolic acidosis: the impact of acute ethanol in hemorrhagic shock. 140 53

Recent studies have suggested that ethanol may exert some of its central depressant actions by increasing the extracellular levels of adenosine in the brain. Ethanol can inhibit the cellular uptake of adenosine, thus increasing its extracellular concentration. After ethanol metabolism by the liver, blood acetate levels are elevated and acetate metabolism in the brain could also lead to the production of adenosine. Rat cerebral cortical cup release experiments failed to reveal any elevation in the extracellular levels of either adenosine or inosine following the intraperitoneal (IP) administration of ethanol (1.5 g/kg) or acetate (2 g/kg). IP-administered ethanol (0.5 and 1.0 g/kg) enhanced the magnitude and duration of the inhibition by iontophoretically applied adenosine of the spontaneous firing of rat cerebrocortical neurons; an action which would be consistent with the block of adenosine uptake. Acetate, applied iontophoretically, depressed the spontaneous firing of 63% of the cerebrocortical neurons tested. 8-p-Sulphophenyltheophylline, an adenosine antagonist, was ineffective at blocking these inhibitions, indicating that adenosine generation is unlikely to have played a major role in the acetate-evoked depression of cerebral cortical neurons.
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PMID:Actions of ethanol and acetate on rat cortical neurons: ethanol/adenosine interactions. 147 11

Histamine and other mediators have been shown to be involved in the ethanol-induced jejunal plasma protein loss. In this study we have investigated whether the histamine (H)-related component of this protein loss is mediated by H1-receptors, H2-receptors or both. Four groups of dogs (n = 12 in each) were studied. They were: untreated, H1 + H2-receptor blockade, H1-receptor blockade and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptors respectively. In all animals, jejunal protein loss was measured over 10 min periods for 90 min. Ethanol increased protein loss in all time periods (p less than 0.001). This protein loss was depressed by H1 + H2-receptors blockade throughout 90 min (p less than 0.01). H1-receptor blockade caused a similar depression of ethanol effect but only during 20 to 40 min (p less than 0.05). In contrast, H2-receptor blockade aggravated the protein losing effect of ethanol throughout 90 min (p less than 0.01). Analyses of data tend to suggest that the ethanol-induced protein loss is mediated principally by H1-receptors, and that a complete inhibition of the histamine-related ethanol-induced protein loss can be achieved only by a simultaneous blockade of both H1 and H2-receptors, and not by H1- or H2-receptor blockade alone.
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PMID:The role of histamine1 and histamine2 receptors in the ethanol-induced jejunal plasma protein loss. 152 91

Moderate ethanol consumption, associated with cardiac depression, occurs in greater than 50% of trauma. Hemorrhagic shock, a significant component of trauma in the clinical setting, causes intrinsic cardiac contractile dysfunction. In this study, we used an isolated heart model to determine whether acute ethanolism increases the cardiovascular risk associated with hemorrhagic shock. We hypothesized that hemorrhagic shock in the acutely intoxicated subject would cause significantly greater cardiac dysfunction compared with that observed in a nonintoxicated subject. A total of 116 guinea pigs was divided into four groups: control (no ethanol, no shock), ethanol intoxication alone (1 mg/kg iv), hemorrhagic shock alone (mean arterial blood pressure, 30 mmHg for 2 h), and a combination of hemorrhagic shock plus ethanol. Half of the hearts in each group were used for isolated heart studies, and half were used to assess myocardial cell membrane integrity. Ethanol alone reduced peak isovolumic pressure by 36%, maximal rate of left ventricular pressure (LVP) rise by 27%, and maximal rate of LVP fall by 35%; however, contractile depression was significantly greater in the intoxicated, hemorrhaged, group compared with the nonintoxicated, hemorrhaged, group (P less than 0.05). Both ethanol and hemorrhage independently altered myocardial cell volume regulation; however, abnormalities in myocardial cell volume regulation induced by hemorrhage were similar in the intoxicated and nonintoxicated groups. Our data show that hemorrhagic shock causes significantly greater cardiac contractile dysfunction in the intoxicated subject.
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PMID:Cardiac contractile effects of ethanolism and hemorrhagic shock. 156 92

Ethylene glycol (EG) is a toxic chemical found in antifreeze and heat exchangers. Standard therapy for EG intoxication in administration of ethanol (ETOH) to inhibit its metabolism by alcohol dehydrogenase (ADH). Studies indicate 1,3-butylene glycol (BG) binds to ADH more efficiently than EG and is orally less toxic than EG or ETOH. Male rats were divided into 5 groups of 6 animals. Groups received by oral intubation a single dose of EG (32 mmole/kg), BG (39 mmole/kg) initially and every 6 h up to 72 h, ETOH (39 mmole/kg) initially and every 6 h up to 72 h, or EG initially and then either BG or ETOH every 6 h up to 72 h. Administration of ETOH produced hepatotoxicity and pulmonary pathology as indicated by changes in clinical chemistry, urinalysis, and histopathology, while BG did not. Neither ETOH nor BG produced any apparent nephrotoxicity. ETOH produced ataxia, lethargy and central nervous system depression while BG did not. BG produced a higher concentration of urinary EG indicating a better inhibition of ADH metabolism of EG. Ethanol produced a higher EG blood concentration than BG. Ethanol's higher EG blood concentration may be partially attributed to dehydration and a decreased urine output as well as inhibition of ADH metabolism. Ethanol produced mortality in all animals prior to 72 h. The EG/ETOH combination produced mortality more quickly due to additive toxicity of the combination. Lack of any significant toxicity produced by BG and the production of significant toxicities by ETOH indicates that BG is potentially a better antidote than ETOH.
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PMID:The toxicokinetics of 1,3-butylene glycol versus ethanol in the treatment of ethylene glycol poisoning. 162 60

Ethanol possesses anxiolytic and anticonflict effect in low dose, but exhibits consciousness depression in higher serum level. It also has addictive effects on benzodiazepines (BZD) and its mechanism has been thought to be closely related to GABA-BZD receptor complex. Flumazenil is a well-known potent antagonist in benzodiazepine intoxication. It can restore the patients' consciousness in case of BZD overdose in comatose condition. In the treatment of ethanol intoxication, flumazenil has not been well-accepted as an antidote. We report a case of severe ethanol intoxication (serum level: 512 mg/dl) with deep coma. Flumazenil 0.5 mg restored her consciousness 90 mins after antidote had been administrated. According to the literature, improvement of conscious level was not due to decay of serum ethanol level but flumazenil itself, which has potential benefit to the condition of ethanol intoxication. This effect is delayed as compared with its using in BZD overdose.
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PMID:[Ethanol intoxication treated with flumazenil: a case report]. 166 90

1. This laboratory has previously reported that pretreatment with ganglioside, or even with its constituent, sialic acid (SA), can attenuate certain intoxicating effects of ethanol. It was important to see if these findings could be replicated, particularly by using other measures of ethanol effects. Herein we report that pretreatment with either gangliosides or SA attenuated ethanol-induced decrements in locomotion, nose-poke exploration, and anxiety, but not body temperature. 2. An ethanol dose of 4 gm/kg caused a temperature drop of about 3 degrees C, which was unaffected by any pretreatment. The onset to sleep, however, was delayed an average of 18 or 36 secs in mice pretreated with ganglioside or SA, respectively. Ethanol-only (4 gm/kg) depressed mean cumulative locomotor activity to 31% of normal, whereas the depression was 83% of normal with beef brain ganglioside pretreatment. At 2 gm/kg ethanol alone decreased nose poking in a hole-board test to 29% of normal, but the depression was only 55-63% of normal with SA or ganglioside pretreatment. In a staircase climbing anxiety test, this dose of ethanol had no effect by itself, but both ganglioside and SA pre-treatment increased climbing by 22%. Ethanol did depress rearing to only 11% of normal, whereas rearing was 51 and 99% of normal with SA and ganglioside pretreatment, respectively. In a dark-preference test, ethanol-only caused mice to spend 64% of the time in the light, compared to 31% for controls. Time in the light was only 39 and 46% with ganglioside and SA pretreatment, respectively. 3. Blood levels of ethanol were not significantly affected by pretreatment. 4. When given alone, gangliosides significantly stimulated locomotion and staircase climbing. SA significantly decreased rearing in the staircase test. Both gangliosides and SA tended to increase nose poking, number of crossings in the dark-preference test, and time in a lighted compartment. Thus, it is possible that some of the attenuation of intoxication is attributable to non-specific stimulant properties of gangliosides and SA.
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PMID:Ganglioside or sialic acid attenuates ethanol-induced decrements in locomotion, nose-poke exploration, and anxiety, but not body temperature. 167 67

The effects of ethanol alone and in combination with sulphanilyl fluoride on some of the antioxidant defences in the stomach of rats have been examined. These effects were correlated with lesion formation in the gastric mucosa. Oral administration of ethanol induced gastric lesions which were prevented by sulphanilyl fluoride pre-treatment. N-Ethylmaleimide antagonized the anti-lesion action of sulphanilyl fluoride. Ethanol administration lowered the glucose-6-phosphate dehydrogenase activity in the gastric mucosa, an effect potentiated by N-ethylmaleimide pre-treatment. The total superoxide dismutase activity was unaffected by the drugs used in the present study. Ethanol, however, markedly increased mucosal catalase activity which was reduced by sulphanilyl fluoride pretreatment and reversed by N-ethylmaleimide. It is concluded that the ulcerogenic mechanism of ethanol is mediated at least in part by the depression of the hexose monophosphate shunt and the production of active oxygen species, whereas the anti-lesion action of sulphanilyl fluoride is probably not mediated through these mechanisms.
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PMID:Ulcerogenic mechanism of ethanol and the action of sulphanilyl fluoride on the rat stomach in-vivo. 168 63

Nucleus locus coeruleus (LC) was sequentially transplanted with hippocampus or cerebellum from rat fetuses to the anterior eye chamber of adult rat hosts. Histological, electrophysiological and pharmacological studies indicate that the LC neurons survive and functionally innervate neurons in hippocampal and cerebellar cografts. Ethanol, when superfused over the double transplants in urethane-anesthetized hosts, caused excitations of hippocampal neuronal activity at doses between 1 and 30 mM, whereas applications above 30 mM depressed the activity of grafted hippocampal neurons. Similar results were observed in cerebellar Purkinje neurons cografted in oculo, except that cerebellar neurons were more sensitive to both the excitatory and the depressant effects of ethanol. The excitations caused by lower ethanol doses in double grafts were prevented by the cosuperfusion of 0.5 to 1.0 microM clonidine, a treatment which effectively removed the inhibitory influence of the LC neurons from the grafted neuronal circuit by depressing the LC neuronal activity. Ethanol-induced excitations were also not observed in single grafts of hippocampus, which lack a catecholamine innervation. Furthermore, in double grafts, when the noradrenergic inhibition was blocked postsynaptically with the alpha adrenergic antagonist phentolamine, ethanol-induced excitations were prevented, although ethanol did not alter the postsynaptic actions of norepinephrine. Our data suggest that the ethanol-induced excitations in the cerebellar and hippocampal grafts appear to be disinhibitions mediated by an ethanol-induced depression of the inhibitory noradrenergic input to these target tissues from LC cografts. Indeed, the doses of ethanol that induced neuronal excitations in hippocampal transplants also elicited marked depressions of LC neurons.
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PMID:Electrophysiological effects of ethanol on hippocampal and cerebellar neurons cografted with locus coeruleus in oculo: role of the noradrenergic circuitry. 173 30


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