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)

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

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

Infections and chronic liver injury are common causes of morbidity and mortality in alcoholics, and both of these may be related to an altered immune response. This study describes a guinea pig model of chronic ethanolism designed to selectively study the cellular immune system in a setting free from the malnutrition, socioeconomic deprivation, and severe underlying hepatic dysfunction seen in human disease. Animals were given 2.5 g/kg/day of ethanol as a 15% solution in 0.9% NaCl or isocaloric-dextrose-saline control solution intraperitoneally in 2 divided doses for 5 weeks. At 2 weeks, the mean serum ethanol level 1 hr after treatment was 20.4 mM (range 8.9-30.6) while the mean serum acetaldehyde level was 55.1 microM (range 17.0-111). At 5 weeks the serum levels for ethanol and acetaldehyde were 20.1 mM (13.3-32.9) and 41.5 microM (2.4-87.6), respectively. Weight gain was persistent throughout the study and did not differ significantly between ethanol and control groups. After 5 weeks of treatment, lymphocyte response to the mitogens, phytohemagglutinin, and concanavalin A was significantly decreased in the ethanol treated group (p less than 0.05). Response to the specific antigen, picrylated human serum albumin, T & B cell per cent and number, skin test reactivity, peripheral white blood cell count, total lymphocyte count, and migration inhibitory factor production were not significantly altered by 5 weeks of ethanol treatment. Therefore, in a controlled animal model of chronic ethanolism, we observed a significant depression of lymphocyte blastogenic response which may, in part, explain the increased propensity to infection by intracellular pathogens seen in alcoholics.
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PMID:Ethanol-induced alterations in lymphocyte function in the guinea pig. 637 25