This study was undertaken to assess the contribution of fat embolism (FE) to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock and FE (HR/FE), resuscitated hemorrhagic shock, FE, and control. FE was induced via intramedullary femoral canal pressurization using a 1–1.5 ml bone cement injection. Only HR/FE animals displayed significant proinflammatory cytokine release as compared to controls. These findings suggest that the combination of resuscitated shock with FE initiates an inflammatory response, which may lead to the development of fat embolism syndrome. The objective of this study was to assess the contribution of fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Only the animals that underwent resuscitated shock and fat embolism displayed amplified BALF proinflammatory cytokine expression. These findings suggest that the combination of resuscitated shock with fat embolism initiates an inflammatory response, which may play a role in the development of fat embolism syndrome. Only HR/FE BALF IL-8 and MCP-1 levels were significantly higher than controls (0.72 ng/ml vs. 0.26ng/ ml, p=0.03; 18.3 ng/ml vs. 2.0 ng/ml, p=0.01, respectively). Twenty-seven NZW rabbits were randomly assigned into four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Shock was induced via carotid bleeding for one-hour prior to resuscitation. For FE induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. Four hours later, postmortem bronchoalveolar lavage was performed through the right mainstem bronchus. Analyses of bronchoalveolar lavage fluid (BALF) of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) were carried out in triplicate and blinded fashion using the ELISA technique. Our findings suggest that FE by itself does not initiate inflammatory lung injury, as there were no apparent differences between the control and FE cytokine levels. Only the HR/FE animals revealed elevated levels of pro-inflammatory cytokines in BALF. These findings are in agreement with our previous results, which displayed neutrophil activation only in the HR/FE group.
