Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
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Exp. Toxicol. Pathol. · Nov 2002
Polymicrobial sepsis induces organ changes due to granulocyte adhesion in a murine two hit model of trauma.
Polytrauma patients, who develop organ dysfunction, have often undergone multiple subsequent insults ("hits"). The sequence of organs that show a dysfunction mostly is lung, liver, kidney and heart. The aim of the present study was to investigate whether a second hit after trauma induces organ changes. Furthermore, it was of interest to identify possible pathogenic mediators such as polymorphonuclear granulocytes (PMN) and cytokines. For this purpose, a two hit model of systemic damage in mice was developed. Sepsis was induced by caecal ligation and puncture (CLP), which was preceded 48 hours by a femur fracture, the most common fracture of long bones in trauma patients. This fracture was combined with a haemorrhagic shock. ⋯ A new rodent model mimicking the situation in the polytraumatized patient was developed. Although the animals showed minimal organ manifestation, a high percentage died probably due to cytokinemia. Furthermore, the increased TNF-alpha levels may lead to increased adhesion of PMN in the lung venules. This adhesion developed four days after the second hit. This might be the initial step for the development of extensive lung lesions in later phases. This model represents the SIRS more than MODS. This is a model for devolopment of posttraumatic disease due to cytokinemia and less for chronic multiple organ dysfunction and failure.