Article date: January 0001
By: B Relja, C Höhn, F Bormann, K Seyboth, D Henrich, I Marzi, M Lehnert in Volume 165, Issue 4b, pages 1188-1199
BACKGROUND AND PURPOSE
Haemorrhagic shock and resuscitation (H/R) induces hepatic injury, strong inflammatory changes and death. Alcohol intoxication is assumed to worsen pathophysiological derangements after H/R. Here, we studied the effects of acute alcohol intoxication on survival, liver injury and inflammation after H/R, in rats.
EXPERIMENTAL APPROACH
Rats were given a single oral dose of ethanol (5 g·kg−1, 30%) or saline (control), 12 h before they were haemorrhaged for 60 min and resuscitated (H/R). Sham groups received the same procedures without H/R. Measurements were made 2, 24 and 72 h after resuscitation. Survival was assessed 72 h after H/R.
KEY RESULTS
Ethanol increased survival after H/R three‐fold and also induced fatty changes in the liver. H/R‐induced liver injury was amplified by ethanol at 2 h but inhibited 24 h after H/R. Elevated serum IL‐6 levels as well as hepatic IL‐6 and TNF‐α gene expression 2 h after H/R were reduced by ethanol. Ethanol enhanced serum IL‐1β at 2 h, but did not affect increased hepatic IL‐1β expression at 72 h after H/R. Local inflammatory markers, hepatic infiltration with polymorphonuclear leukocytes and intercellular adhesion molecule 1 expression decreased after ethanol compared with saline, following H/R. Ethanol reduced H/R‐induced IκBα activation 2 h after H/R, and NF‐κB‐dependent gene expression of MMP9.
CONCLUSIONS AND IMPLICATIONS
Ethanol reduced H/R‐induced mortality at 72 h, accompanied by a suppression of proinflammatory changes after H/R in ethanol‐treated animals. Binge‐like ethanol exposure modulated the inflammatory response after H/R, an effect that was associated with NF‐κB activity.
DOI: 10.1111/j.1476-5381.2011.01595.x
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