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1 Surgery, University of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: Irshad.Chaudry{at}ccc.uab.edu.
Although systemic interleukin-6 (IL-6) level is elevated, hepatocellular function is impaired and liver injury occurs following trauma-hemorrhage (T-H), it remains unknown whether a causal relationship exists between elevated IL-6 levels and liver injury after T-H. We hypothesized that IL-6 is causative in the development of hepatic dysfunction and injury following T-H. To examine this, adult male Sprague-Dawley rats underwent a 5 cm midline laparotomy and were subjected to hemorrhagic shock (BP = 35 mmHg for ~ 90 min), followed by resuscitation (Ringers lactate, 4X the shed blood volume). At 2, 5 and 24 h thereafter, blood samples were collected, the liver isolated, and perfused for 60 min. Portal inflow pressure was measured and perfusate samples collected to measure IL-6, alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels. A significant positive correlation between plasma levels of IL-6 and ALT and perfusate levels of IL-6 and LDH levels was observed. In a second series of experiments, rats were treated with immunoglobulin G (IgG) or antibodies against rat IL-6 (anti-IL-6) at the onset of resuscitation. At 5 hr after resuscitation, anti-IL-6 treatment attenuated the T-H induced increases in plasma ALT and thromboxane B2 (a thromboxane A2 metabolite) levels and bile flow was normalized to sham levels. Perfusion of livers from normal rats with IL-6 did not alter portal pressure; however, perfusion of a stable thromboxane A2 analog dose-dependently increased portal pressure. Thus, IL-6 plays a significant role in the induction of hepatic dysfunction and liver injury following T-H that appears to be in part mediated by increased thromboxane A2 levels.
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