Alcoholism, clinical and experimental research
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Alcohol. Clin. Exp. Res. · Apr 2002
Interleukin-4 treatment restores cellular immunity after ethanol exposure and burn injury.
Previous studies from this laboratory showed that the suppression of cell-mediated immunity after the combined injury of ethanol exposure and burn is mediated by increased presence of the proinflammatory cytokine interleukin (IL)-6. IL-4 is a T-helper cell type 2 lymphocyte-derived cytokine that serves to down-regulate the inflammatory response. Therefore, the goal of this study was to evaluate the effects of ethanol exposure and burn injury on lymphocyte production of IL-4 and to determine whether administration of IL-4 could improve cellular immunity after ethanol exposure and burn injury through modulation of IL-6 levels. ⋯ These studies suggest that the loss of lymphocyte production of IL-4 after ethanol exposure and burn injury may contribute to the exaggerated production of IL-6, a known mediator of immune suppression after injury. Moreover, the administration of IL-4 may be beneficial for patients with injuries that are characterized by a dysregulated inflammatory response.
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Alcohol. Clin. Exp. Res. · Jan 2002
Alcohol consumption attenuates febrile responses to lipopolysaccharide and interleukin-1 beta in male rats.
Chronic and acute alcohol use exert profound modulatory effects on the immune system which manifest as impaired host defense against infections. An important feature of this response is the interaction between the immune and the central nervous systems. This study investigated the effects of 14 days of alcohol exposure on cytokine-mediated neuroimmune interactions that affect the febrile component of the host-defense response. ⋯ The attenuated LPS- and IL-1beta-induced febrile responses in EtOH-consuming rats and the corresponding deficit in hypothalamic production of IL-1beta suggest that alcohol may impair IL-1beta-mediated neuroimmune communication.
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Alcohol. Clin. Exp. Res. · Nov 2001
Effects of abstinence on the brain: quantitative magnetic resonance imaging and magnetic resonance spectroscopic imaging in chronic alcohol abuse.
Structural brain damage, especially to white matter, is well documented in chronic alcohol abuse. There is also evidence for brain metabolic abnormalities in this condition. It is unknown, however, to what extent these structural and metabolic changes are present in treated alcohol abusers who achieve long-term abstinence versus treatment-naïve, heavily drinking individuals. ⋯ White and gray matter volumes in different regions of the brain were greater or smaller in recovering, treated alcoholics. The findings suggest region-specific structural recovery from chronic alcohol-induced brain injury, but also region-specific long-term structural damage in abstinent alcoholics. White matter lesions were widespread in active drinkers and may partly resolve during long-term abstinence. Proton MR spectroscopic measures, as applied in this cross-sectional study, were largely ineffective in revealing metabolic effects of abstinence on the alcohol-damaged brain.
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Alcohol. Clin. Exp. Res. · Sep 2001
Randomized Controlled Trial Comparative Study Clinical TrialDivalproex sodium in alcohol withdrawal: a randomized double-blind placebo-controlled clinical trial.
Divalproex sodium, an anticonvulsant and antikindling agent and gamma-aminobutyric acid enhancer, has been proposed as an alternative to benzodiazepines for treating alcohol withdrawal. This study reports on a randomized, double-blind, placebo-controlled trial of divalproex sodium in acute alcohol withdrawal. ⋯ This placebo-controlled pilot study suggests that divalproex sodium significantly affects the course of acute alcohol withdrawal and reduces the need for treatment with a benzodiazepine. A more aggressive loading dose strategy may demonstrate a more robust or earlier response.
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Alcohol. Clin. Exp. Res. · Jun 2001
Effects of ethanol and naltrexone in a model of traumatic brain injury with hemorrhagic shock.
Ethanol predisposes to traumatic injury and causes respiratory depression and cardiovascular compromise in models of traumatic brain injury (TBI) and hemorrhagic shock (HS). Endogenous opioids may play a role in ethanol intoxication and TBI. We studied the effects of ethanol and the opiate antagonist agent naltrexone (NTX) in a TBI/HS model. ⋯ In this TBI/HS model, NTX reverses ethanol-induced depression of hypercapnic ventilatory response but does not improve MAP, CPP, or metabolic acidosis. This suggests that the respiratory effects of ethanol in TBI, but not the hemodynamic effects, may be mediated by opiate receptor activation.