INFLAMMATORY ALTERATIONS IN A NOVEL MODEL OF COMBINED BLUNT CHEST TRAUMA AND HEMORRHAGIC SHOCK

Abstract

Blunt chest trauma frequently occurs in severely injured patients and is often associated with hemorrhagic shock (hem). Clinical studies indicate that the prognosis of severely injured patients worsens, if chest trauma is part of the trauma pattern. Although it is possible that inflammatory effects contribute to the adverse outcome, the immunological alterations of this combined injury remain unclear. The aim of the present study, therefore, was to establish a model of blunt chest trauma combined with hem and to evaluate the resulting Kupffer cell inflammatory response. In this regard, Kupffer cells are known to contribute to inflammation following trauma-hemorrhage as well as blunt chest trauma. Male C3H/HeN mice were anesthetized, instrumented and subjected to sham procedure, chest trauma (single blast wave), hem (60 min, 35 ± 5 mmHg, resuscitated with saline 4 × shed blood volume) or combined chest trauma + hem. 20 hrs later, Kupffer cells were isolated, stimulated (1 μg/ml LPS for 24 hrs) and TNF-α, IL-6, IL-10 and MIP-2 release were measured by ELISA.TableThis novel model did not induce mortality in combined chest trauma with pressure-controlled hem. Kupffer cell inflammatory mediator production was significantly elevated following chest trauma alone. Subsequent hem slightly enhanced cytokine and chemokine release. These findings indicate that isolated blunt chest trauma caused marked Kupffer cell activation comparable to hem alone and that a combination of these insults moderately intensified the inflammatory response. (DFG KN 475/2-1)