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)

Ethylene glycol butyl ether, CAS 111-76-2, an ingredient in many popular commercial window/glass cleaners, is known to produce equal if not greater toxicity than ethylene glycol when administered to animals. Treatment recommendations for human poisonings are based upon animal data and include the use of ethanol therapy to inhibit the production of toxic metabolites. No human experiential data exist to accurately assess human toxicity or to verify treatment modalities. A 5 month retrospective review of all glass cleaner ingestions reported to a regional poison information center disclosed 24 pediatric patients, ages 7 mo to 9 y, who ingested 5-300 mL of a liquid glass cleaning product containing ethylene glycol butyl ether. All ingestions were reported within 5 min of ingestion, and all 24 children were asymptomatic at that time and subsequently. The product concentrations of ethylene glycol butyl ether ranged from 0.5% to 9.9%. Two of the 24 children ingested > 15 mL and were treated by gastric emptying and 24 h hospital observation. Neither hospitalized child suffered symptoms consistent with hemolysis, nervous system depression, acidosis, or renal compromise. Dilution with oral fluids at home is considered appropriate treatment of pediatric ingestions of < 10 mL of a commercial liquid glass/window cleaners containing < 10% ethylene glycol butyl ether.
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PMID:Clinical evaluation of pediatric ethylene glycol monobutyl ether poisonings. 835 28

To determine the effects of moderate ethanol consumption on the mechanical, biochemical, and structural characteristics of the heart, myocardial mechanical performance, contractile protein enzyme activity, and the number and size of myocytes were measured in male Fischer 344 rats after the ingestion of 30% oral ethanol. Papillary muscles removed from the left ventricle were greater in length, weight, and cross-sectional area than the corresponding muscles from the right side. However, no differences were found between control and ethanol-treated myocardium when either the left or right side was compared separately. Chronic ethanol ingestion resulted in an increase in resting tension in left ventricular muscles, with no alteration in peak developed tension. Moreover, time to peak tension was significantly prolonged, whereas a depression was observed in the peak rate of isometric tension development. Isotonically, left muscles from ethanol-treated rats revealed a prolongation of time to peak shortening and a marked depression in the velocity of shortening at physiological loads. No changes were noted in muscles from the right ventricle. Contractile protein enzyme activity revealed no differences in myofibrillar Mg(2+)-ATPase activity in right and left ventricular myocardium between control and ethanol-treated rats in the presence of EGTA. However, at physiological activating levels of calcium, an upward shift of the myofibrillar Mg(2+)-ATPase activity-calcium curve occurred in left myocardium, whereas a depression in this relation was seen in the right ventricle. As a result of chronic ethanol intake, a decrease was noted in the volume percent of myocardium occupied by myocytes, and that myocyte cell volume per nucleus was found to remain essentially constant throughout the various layers of the ventricular wall. Importantly, a 14% significant decrease in the total number of myocyte nuclei was demonstrated in the left ventricular myocardium of rats on chronic ethanol consumption. Thus, chronic but moderate alcohol ingestion resulted in depressed contractile performance, alterations in myofibrillar Mg(2+)-ATPase activity, and myocyte loss. These events may serve to function as preliminary indicators of the onset of heart failure of alcoholic origin in this animal model.
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PMID:Myocardial mechanical, biochemical, and structural alterations induced by chronic ethanol ingestion in rats. 138 62

The present article summarizes some comparative studies of the Fawn-Hooded (FH) rat, a potential animal model of ethanol preference, and the Flinders Sensitive Line (FSL) rat, a potential animal model of depression. Both FH and FSL rats exhibit high degrees of immobility in the forced swim test and have difficulty learning a two-way active avoidance task. However, there were no differences between the FH and FSL rats in the elevated plus maze. Studies of ethanol preference indicated high rates of ethanol intake (greater than 4 g/kg) and preference (greater than 50%) in the FH rats, but low rates of ethanol intake (less than 1.1 g/kg) and preference (less than 20%) in FSL rats. It is concluded that the FSL rats exhibit behaviors consistent with their being an animal model of depression, whereas the FH rats exhibit features consistent with their being an animal model of both depression and alcoholism. Psychopharmacological challenges indicated that both FSL and FH rats were more sensitive to the hypothermic effects of oxotremorine, a muscarinic agonist. However, FSL rats were also more sensitive to serotonergic agonists, and some of the present results and other investigators have reported serotonergic subsensitivity in the FH rats. Thus, FSL rats exhibit both cholinergic and serotonergic supersensitivity, whereas FH rats exhibit cholinergic supersensitivity but normal or reduced serotonergic sensitivity. Progeny from a genetic cross between FH and FSL rats exhibit cholinergic supersensitivity and have high ethanol preference scores. These data are consistent with genetic models suggesting that ethanol preference may be influenced by dominant genes, whereas cholinergic sensitivity may be influenced by recessive genes.
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PMID:Genetic animal models of depression and ethanol preference provide support for cholinergic and serotonergic involvement in depression and alcoholism. 138 57

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

Eighty-two women, presenting as normal-weight bulimics, obese binge eaters, social phobics, and individuals with panic disorder, were compared on anxiety, depression, and substance abuse. All were administered the Anxiety Disorder Interview Schedule-Revised and completed the Michigan Alcohol Screening Test, Drug Abuse Screening Test, and Self-Consciousness Scale. A striking proportion of eating disorder subjects were comorbid for one or more anxiety disorders, the most frequent diagnoses being generalized anxiety disorder and social phobia. The results suggest that the place of anxiety in bulimia nervosa goes beyond that discussed within the context of the anxiety reduction model. Conflicting comorbidity findings among this and prior investigations are noted, however, and discussed in terms of the issue of differential diagnosis between eating and anxiety disorders.
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PMID:Comparison of bulimics, obese binge eaters, social phobics, and individuals with panic disorder on comorbidity across DSM-III-R anxiety disorders. 143 Jun 7

Flumazenil is effective in reversing sedation resulting from benzodiazepine (BZD) toxicity. Its use for other causes of sedation have not been well described. A 23-y-old male was found unconscious. Upon being aroused, the patient stated he had recently ingested 1 1/2 bottles of vodka/beer and 250 mg of diazepam. Physical examination revealed shallow breathing and respiratory depression. Arterial blood gases were consistent with the clinical diagnosis of respiratory depression (pH 7.34, pCO2 47, pO2 99). However, after receiving 3 mg of flumazenil, the respiratory depression improved so that the patient no longer required intubation. The drug screen returned negative for BZDs and the patient had a blood alcohol level of 332 mg/dl. He later denied BZD use. The patient's clinical course improved throughout the study period, and mechanical ventilation was avoided. This report reflects a possible role for flumazenil in reversing the respiratory depression produced by ethanol ingestion.
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PMID:Reversal of ethanol-induced respiratory depression by flumazenil. 145 8

Experiments on rats subjected to forced alcoholization for 5.5 days were made to measure the content of ethanol, acetaldehyde and ketone bodies in the blood during intoxication and 2 days after ethanol withdrawal and to estimate the intensity of postintoxication disorders in heart activity on the third day after alcoholization withdrawal. A positive correlation was discovered between depression of left ventricular contractility and the blood content of acetaldehyde and ketone bodies. The magnitude of the threshold of heart fibrillation did not correlate well with the concentration of ethanol during alcoholization. However, it agreed well with ethanol concentration in the postintoxication period. Additional administration to the animals of beta-hydroxybutyrate or caprylic acid in the postintoxication period intensified heart contractility depression. The conclusion is drawn that elimination of ketosis in ethanol withdrawal as well as a progressive taking out of alcoholic patients from dipsomania can prevent the development or attenuate the intensity of postintoxication heart injury.
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PMID:[The role of ketone bodies in the development of postalcoholic-intoxication heart damage in rats]. 145 94

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.
Alcohol
PMID:Actions of ethanol and acetate on rat cortical neurons: ethanol/adenosine interactions. 147 11

Essential tremor (ET), more common than Parkinson's disease (PD), has commonly been considered "benign." This investigation compared diagnostic characteristics, patient satisfaction with treatment, and psychosocial complications between a group of male patients treated for essential tremor and a group of male parkinsonian patients. Those who had ET tended to be more commonly misdiagnosed than those with PD. Fewer ET patients were satisfied with response to treatment than PD patients. Both groups equally expressed embarrassment about their condition, and both perceived similar difficulties with common activities of daily living and social situations. There were no significant differences between ET and PD patients for history of ethanol use or pharmacotherapy for anxiety or depression.
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PMID:Severe essential tremor compared with Parkinson's disease in male veterans: diagnostic characteristics, treatment, and psychosocial complications. 150 24

3-alpha-Hydroxy-5-beta-pregnan-20-one [pregnanolone (PA)] and 3-beta-hydroxy-5-pregnen-20-one 3-sulfate [pregnenolone sulfate (PS)] are steroids that have been shown in biochemical studies to be active at the GABA-benzodiazepine-chloride receptor complex, Pa as a "barbiturate-like" agonist and PS as a "picrotoxin-like" antagonist. Since other compounds that are active at this site interact with the effects of pentobarbital and ethanol, the behavioral effects of these steroids alone and in combination with pentobarbital and ethanol were tested. Pa blocks the convulsions caused by pentylenetetrazole (PTZ) and increases motor activity when given alone in low doses. In combination with either pentobarbital or ethanol, it enhances the depression in motor activity, hypothermia, and hypnosis. In contrast, PS has no effect on PTZ convulsions and depresses motor activity by itself. With pentobarbital, PS enhances the depression in motor activity but has no effect on hypothermia or hypnosis. With ethanol, PS enhances the hypothermia but does not affect motor activity or hypnosis. Therefore, Pa and PS show different but not opposite effects in interacting with compounds active at the GABA-benzodiazepine-chloride receptor complex.
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PMID:Interaction of pregnanolone and pregnenolone sulfate with ethanol and pentobarbital. 151 42


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