Effects of trace element supplementation on the inflammatory response in a rabbit model of major trauma.

Patients with a severe trauma exhibit a strong oxidative stress, an intense inflammatory response, and long-lasting hypermetabolism, all of which are proportional to the severity of injury. In this study, we investigated the impact of trace element (TE) supplementation on the inflammatory response in an animal model of major trauma. New Zealand White rabbits were randomly assigned as a control group (n=5) and an experimental group (n=70) that, after receiving a major trauma, was subdivided into Trauma-Control (n=35) and Trauma-TE (n=35) groups. Systemic inflammatory response syndrome (SIRS) was observed in 40 out of 70 rabbits with a trauma, with a higher incidence in the Trauma-Control group (88.6%; 31/35) than the Trauma-TE group (28.6%; 10/35) (p<0.01). The mortality rate was significantly different between the Trauma-Control and the Trauma-TE groups; (34% vs. 8%; p<0.01). There were significant post-trauma alterations in the levels of (1) serum and spleen zinc (Zn), copper (Cu), selenium (Se), and manganese (Mn), (2) serum AST and ALT, (3) serum interleukin-6/10, and (4) nuclear factor kappa binding (NF-kappaB) activity and the expression. TE supplementation: (1) improved blood urea nitrogen (BUN), and creatinine (Cr) levels, (2) stabilized IL-6/10 production, (3) decreased NF-kappaB p(65) production. Appropriate TE supplementation can improve the TE status, mitigate SIRS, and reduce the mortality due to multiple organ dysfunction syndromes (MODS)/multiple organ failure (MOF) after major trauma.