Abstract
Acute ethanol intoxication increases the production of reactive oxygen species (ROS). Hemorrhagic shock with subsequent resuscitation (H/R) also induces ROS resulting in cellular and hepatic damage in vivo. We examined the role of acute ethanol intoxication upon oxidative stress and subsequent hepatic cell death after H/R. 14 h before H/R, rats were gavaged with single dose of ethanol or saline (5 g/kg, EtOH and ctrl; H/R_EtOH or H/R_ctrl, resp.). Then, rats were hemorrhaged to a mean arterial blood pressure of 30 ± 2 mmHg for 60 min and resuscitated. Two control groups underwent surgical procedures without H/R (sham_ctrl and sham_EtOH, resp.). Liver tissues were harvested at 2, 24, and 72 h after resuscitation. EtOH-gavage induced histological picture of acute fatty liver. Hepatic oxidative (4-hydroxynonenal, 4-HNE) and nitrosative (3-nitrotyrosine, 3-NT) stress were significantly reduced in EtOH-gavaged rats compared to controls after H/R. Proapoptotic caspase-8 and Bax expressions were markedly diminished in EtOH-gavaged animals compared with controls 2 h after resuscitation. EtOH-gavage increased antiapoptotic Bcl-2 gene expression compared with controls 2 h after resuscitation. iNOS protein expression increased following H/R but was attenuated in EtOH-gavaged animals after H/R. Taken together, the data suggest that acute EtOH-gavage may attenuate H/R-induced oxidative stress thereby reducing cellular injury in rat liver.
Highlights
Excessive ethanol consumption is one of the leading causes of mortality in the United States [1]
EtOH gavage significantly reduced hepatic 4-HNE at 2 h (31 ± 1%) and 24 h (32 ± 3%) after resuscitation compared to the corresponding control groups after hemorrhagic shock with subsequent resuscitation (H/R) (Figures 1(e)–1(h) and 3(a))
After H/R, acute ethanol gavage reduces proinflammatory changes, hepatic injury as well as mortality rates, effects that may be associated and explained with downregulated NF-κB activation by ethanol in the H/R in vivo model [15]. To further extend these results, we hypothesized that generation of reactive oxygen and nitrogen species (RONS) may be influenced by acute ethanol exposure
Summary
Excessive ethanol consumption is one of the leading causes of mortality in the United States [1]. It is associated with one-third of all traumatic injury deaths per year [2, 3]. Ethanol consumption is associated with increased risk of inflammatory and infectios complications in trauma patients such as pneumonia, sepsis, and multiple organ failure (MOF) and higher morbidity and mortality [7,8,9,10,11,12,13]. Other clinical results show that acute ethanol intoxication is associated with decreased 24 h mortality after trauma (own unpublished data)
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