Altered Levels of Trace Elements in Acute Lung Injury After Severe Trauma

Trace element (TE) supplementation can reduce the incidence of multiple organ failure after severe trauma. The lung plays a main role in post-injury multiple organ failure. In the present study, the relationship between TEs and acute lung injury (ALI) post-injury was investigated in a rabbit model of severe trauma with an injury severity score of 27. New Zealand white rabbits were randomly assigned to trauma-control, trauma-TE groups, and a control group. During days 1-5 post-trauma, each rabbit in the trauma-TE group received 0.1 ml multi-TE compound intraperitoneally to give a daily dose of 32.50 mg/kg of Zn, 6.35 mg/kg of Cu, 1.38 mg/kg of Mn, and 0.16 mg/kg of Se. Concentrations of blood and lung selenium (Se), copper (Cu), zinc (Zn), and manganese (Mn) were measured at 6 and 24 h, as well as 3, 6, 9, and 14 days after trauma. Levels of glutathione peroxidase (GPx), total superoxide dismutase (SOD), Cu/Zn superoxide dismutase (Cu/Zn-SOD), and malondialdehyde (MDA) in serum and lung tissue and the level of intercellular adhesion molecular-1 (ICAM-1) in serum were detected simultaneously. In addition, the lung coefficient (LC) and the lung permeation index (LPI) were measured. Serum and lung Zn, Se, and Mn levels decreased dramatically by 6 h after trauma in both experimental groups. Cu showed no significant changes after trauma. The serum and lung GPx and SOD levels in the experimental group decreased significantly on days 1 and 3, respectively. Serum and lung MDA began to increase on day 3 in the trauma group but increased less after TE supplementation. Serum ICAM-1 peaked on day 6 in the experimental group. LC and LPI increased gradually post-trauma, peaking on days 6 and 9, respectively. In conclusion, an acute lung injury causes declines of the levels of TEs in serum and lung which can be significantly prevented by TE supplementation and which can also mitigate some of the morphological and biomechanical changes in ALI.