Intraperitoneal blood exacerbates the remote inflammatory response to murine peritonitis

Background. This study investigated the effects of intra-abdominal blood on the systemic response to peritonitis using a murine model of hemorrhage, p eritonitis, and multiple organ dysfunction syndrome. Methods. The model used male ICR mice subjected to hemorrhage and intraperi toneal zymosan. Half of the mice received intraperitoneal blood. Outcome me asures included lung myeloperoxidase, lung edema, lung injury score, and pl asma and lung tissue chemokine production. Results. Peritoneal blood (in association with peritoneal inflammation) in- creased lung neutrophil sequestration (myeloperoxidase) (2.56 +/- 1.42 vs. 1.45 +/- 0.49 U/left lung,p = 0.04) and lung weight (0.11 +/- 0.04 vs. 0.07 0.02 g/left lung, p = 0.02), and was associated with significantly higher chemokine levels in plasma (KC and MCP-1) and lung tissue (KC, MIP-2, and M CP-1). Both plasma and lung tissue neutrophil chemoattractants KC and MIP-2 were significantly linearly correlated with myeloperoxidase (p < 0.009), a nd lung tissue KC (a neutrophil chemokine) and MCP-1 and MIP-1 alpha (monon uclear cell chemokines) correlated with lung injury score (p < 0.003). Conclusion. Although blood alone in the peritoneal cavity was well tolerate d, in conjunction with inflammation, it was synergistic in amplifying the s ystemic inflammatory response. The amplified lung injury in this model was associated with significant increases in circulating and lung tissue chemok ine concentrations.