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

Studies of the rate of depletion of serum and tissue methylated and non-methylated folates were carried our in rats maintained for long periods on either a folate deficient (sucrose-water/sulphathiazole) diet or a deficient diet plus high alcohol intake. By means of implantation of a feeding gastrostomy tube, it was possible to sustain constant blood ethanol levels of between 50 and 300 mg/dl for 3-4 weeks with relatively normal calorie intake and without death of the animal. Using this animal model, which closely resembles severe alcoholism in man, a very rapid depression in serum 5-methyl tetrahydrofolate was observed similar to that reported in alcoholic man. At the same time, release of folates from liver stores was umimpaired by alcohol ingestion. Liver folate store depletion rates were identical for alcoholic and folate starved animals. The explanation for the sudden alcohol suppression of serum folate levels must, therefore, be sought at a point in the internal metabolic sequences of folate other than the delivery of folate stores to plasma.
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PMID:The effect of diet and alcohol on the development of folate deficiency in the rat. 120 Dec 37

Intracranial hypertension and brain hydration were scrutinized during acute ethanolism for consideration in the combined head injury setting. Intraventricular pressures and whole brain water levels rose with moderate or high ethanol dosages. The most prominent alterations were associated with respiratory acidosis and hypoxia; less marked changes were found in their absence and point to a second mechanism. Elevated central venous pressures appeared as well in some instances to constitute a third action. It is accordingly suggested that ethanol may add significantly to the combined pathology with associated acute head injury in several ways. These include: contributions to edema formation, to respiratory depression, and to alterations in local hemodyamics.
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PMID:Changes in intracranial pressure and brain hydration during acute ethanolism. 123 77

This paper reports findings relative to a simple, rapid and reproducible technique for the induction of physical dependence upon ethanol in the rat. The dependence was induced by intragastric intubation of 20% (w/v) ethanol solutions at 9-15 g/kg in 3-5 fractional doses daily for 4 days, maintaining blood ethanol concentrations above a threshold level sufficient to sustain observable sedation throughout the entire period of intubation. Two phases were distinguished during the withdrawal period: 1. Prodromal detoxication, characterized by a spectrum of signs and responses of diminishing severity, related to the decline in blood ethanol concentrations (mg/dl): death, greater than 640; coma, 780-460; loss of righting reflex, 640-400; ataxia 3-1, 570-250; sedation 340-190; neutrality, 220-130; 2. Ethanol dependence, characterized by a spectrum of withdrawal signs and reactions of progressively increasing severity as blood ehtanol concentration approached 100 mg/dl: hyperactivity, tremors, akinesia, spastic rigidity, and induced and spontaneous convulsions. A rapid sucession of two diverse clusters of signs and reactions represents a reversal of the central nervous system function from the extremes of ethanol intoxication (CNS depression) to the extremes of ethanol dependence (CNS hyperexcitability) during the withdrawal period. Both extremes may terminate in death.
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PMID:Induction of physical dependence upon ethanol and the associated behavioral changes in rats. 123 14

The effect of prolonged adminstration of ehtanol on cardiac metabolism, contractility, and ultrastructure was investigated. Dogs received 400 ml of a 25 percent solution of ethanol during a period of 3-6 months. Repeated heart muscle biopsied revealed a significant diminution in the activity of intramitochondrial NAD-linked isocitrate dehydrogenase in the animals exposed to alcohol. Oxidative, phosphorylation of mitochondria was measured polarographically using a vibrating oxygen electrode; respiratory control index and mitochondrial oxygen consumption were markedly reduced (p less than 0.001). Myocardial ATP content was significantly diminished (p less than 0.025). Electron microscopic changes observed consisted of mitochondrial degeneration, dehiscence of intercalated discs, and dilatation of intercellular spaces. The average force velocity curve was shifted downward and to the left in afterloaded contractions with a significant depression of Vmax (p less than 0.01). Both calcium binding and calcium uptake of mitochondria and sarcoplasmic reticulum were inhibited. These results suggest that a disorder in the generation of energy and a defect in calcium binding by subcellular membranes may be the determinant events leading to impaired myocardial function in the course of chronic alcoholism.
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PMID:Mitochondrial function and excitation-contraction coupling in the development of alcoholic cardiomyopathy. 123 22

Urea and other small amides cross the toad urinary bladder by a vasopressinsensitive pathway which is independent of osmotic water flow. Amide transport has characteristics of facilitated transport: saturation, mutual inhibition between amides, and selective depression by agents such as phloretin. The present studies were designed to distinguish among several types of transport including (1) movement through a fixed selective membrane channel and (2) movement via a mobile carrier. The former would be characterized by co-transport (acceleration of labeled amide flow in the direction of net flow of unlabeled amide), the latter by counter-transport (acceleration of labeled amide flow in the opposite direction). Mucosal to serosal (M leads to S) and serosal to mucosal (S leads to M) permeabilities of labeled amides were determined in paired bladders. Unlabeled methylurea, a particularly potent inhibitor of amide movement, was added to either the M or S bath, while osmotic water flow was eliminated by addition of ethylene glycol and ethanol could not be demonstrated. Methylurea did not alter water permeability or transmembrane electrical resistance. The demonstration of co-transport is consistent with the presence of ADH-sensitive amide-selective channels rather than a mobile carrier.
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PMID:Amide transport channels across toad urinary bladder. 125 4

A voltammetry technique has been used to determine changes in dopamine release in the rat corpus striatum after two doses of ethanol administration. The dopamine oxidation current reached a maximal value at 30 min after the first alcohol dose with a subsequent decrease towards the initial level at 60 min and kept to the basal level with a statistically insignificant oscillation. When a second dose of alcohol was applied at 60 min, it was followed by a decrease of the dopamine oxidation current peak to 50% of the initial value after another 60 min observation. The results resemble the known effect of alcohol on human behaviour (excitation followed by depression).
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PMID:Effect of acute alcohol treatment on dopamine concentration in corpus striatum of rats: a voltammetric study. 128 81

The effects of 5-hydroxytryptamine (5-HT; given i.p. in doses of 1 or 10 mg/kg) on gastric secretion and mucosal blood flow (GMBF) and on ethanol-induced gastric mucosal damage were studied in rats over a period of 30-450 min. The blood pressure was also examined, in relation to the changes in GMBF. 5-HT, 10 mg/kg, given 30 min before ethanol administration markedly worsened lesion formation and this potentiating action was present for a further 90 min; a significant protective effect was seen only at 450 min after 5-HT injection. The lower dose of 5-HT, 1 mg/kg, did not affect the severity of gastric damage. 5-HT (10 mg/kg) also decreased GMBF at 30 min after injection and this lasted up to the end of 120 min, but the depressive action of ethanol on GMBF was reversed at 450 min. The basal gastric secretory volume was depressed from 30 to 120 min but acid output fell from 75 to 120 min after the higher dose of 5-HT; this reduction of acid secretion was followed by an increase from 360 to 450 min. 5-HT decreased the mean blood pressure in a dose- and time-dependent manner. The heart rate was unaffected by either dose level of 5-HT. The present study not only demonstrates the ulcerogenic action of 5-HT but also the protective nature of the amine. The reduction in secretory volume and lesion formation, but not acid secretion, seems to be related to GMBF depression, whereas the protective action depends on the maintenance of GMBF.
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PMID:Time course study on the action of 5-hydroxytryptamine on gastric secretion and mucosal blood flow and on ethanol-induced gastric mucosal damage in rats. 128 76

The influence of ethanol upon dynamics of rotatory (RN) and post-rotatory nystagmus (PRN), trunk pose-tonic reflexes and their vegetative (cardiac, respiratory) components was studied in chronic experiments on rabbits with the help of electronystagmo- and electromyography. Ethanol was administered once intra-abdominally (1 g/kg) and one time a day during 30 days. Alcohol concentration in blood was determined by gas-and-fluid chromatography. The animal which were given isotonic solution of sodium chloride in the same doses and quantities served as a control group. It was established that vestibular oculomotor reflexes are mainly facilitated in an acute period of ethanol administration, then their inhibition occurs. Besides, the changes of PRN are stronger expressed than those of RN. Labyrinth pose-tonic reflexes are more often inhibited under the influence of ethanol; their strongest depression was observed during the first hour after ethanol administration and on the 15th day of chronic alcoholization. In alcoholization the changes of vestibular-vegetative reaction occur; primary short-term weakening of vestibular influences upon cardiac rhythm and respiration with their subsequent increasing.
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PMID:[The effect of alcohol (ethanol) on the reactions of the vestibular system]. 130 40

In this prospective, 1-year study, 360 males admitted to an inpatient alcoholism treatment program were administered a DSM-III compatible structured interview and subtyped by co-occurring psychiatric disorder. Forty percent satisfied diagnostic criteria for alcohol dependence while 27% met criteria for alcohol dependence and one additional psychiatric syndrome. The dually diagnosed patients were divided into: alcohol dependence plus drug abuse, alcohol dependence plus antisocial personality and alcohol dependence plus depression. These subtypes were compared on multiple dimensions at intake and at 1-year follow-up. At follow-up, all groups showed significant improvement in drinking and psychosocial functioning. The results suggest that subtyping alcoholics by co-morbid psychiatric disorders may be a good postdictor of clinical history, but a poor predictor of drinking outcome.
Alcohol Clin Exp Res 1992 Feb
PMID:Outcomes of co-morbid alcoholic men: a 1-year follow-up. 131 61

This study examines factors related to mortality and 10-year posttreatment functioning for a sample of alcoholic patients who return to their families after an index residential treatment episode. Of the 113 patients followed 2 years after treatment, 20 had died by the time of the 10-year follow-up. Mortality risk was greater among patients who, prior to treatment, consumed more alcohol and were unemployed. Mortality was more strongly associated with medical conditions, liver problems, medication use and lack of confidants assessed 2 years posttreatment. The course for the surviving patients between the 2-year and 10-year follow-ups was one of improvement in terms of alcohol consumption, relative stability in terms of physical symptoms and depression, and an aging-related decline in social activities and employment. Life context and coping factors assessed 2 years after treatment were predictive of long-term outcome. Persons in less stressful life situations, in more cohesive and organized families, and who more frequently used active cognitive coping responses at the 2-year follow-up tended to function better at the 10-year follow-up. Overall, the findings support the value of embedding long-term follow-up studies in a theory of the disorder that is the target of the intervention.
J Stud Alcohol 1992 Mar
PMID:The long-term course of treated alcoholism: II. Predictors and correlates of 10-year functioning and mortality. 131 35


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