This study was undertaken to assess the contribution of pulmonary fat embolism to systemic platelet activation in a rabbit model of fat embolism. Fifteen NZW rabbits were randomly assigned into one of two groups: fat embolism and control. Fat embolism was induced via intramedullary canal pressurization with a 1–1.5 ml bone cement injection. Only the animals that underwent fat embolism displayed consistent platelet activation, as demonstrated by platelet degranulation and procoagulatory surface expression. These findings suggest that fat embolism plays a role in platelet activation and in the overall activation of hemostasis following trauma.

The objective of this study was to use a recently developed rabbit model of fat embolism to assess the systemic hemostatic response to pulmonary fat embolism.

Our findings demonstrate platelet activation following forced liberation of bone marrow contents into the circulation only in the FE group, as demonstrated by CD62P elevation (a marker of platelet degranulation) and annexin V elevation (a marker of procoagulatory surface expression). Platelet activation also coincided with significantly lower platelet counts in the FE group at two and four hours post embolism, suggesting platelet aggregation.

These findings suggest that fat embolism plays a role in platelet activation and in the overall activation of hemostasis following trauma.

Platelet count decreased significantly at two and four hours post knee manipulation only in the FE group. Annexin V expression increased significantly in the FE group at two and four hours post knee manipulation. Lastly, CD62P expression only increased significantly in the FE group at two hours post knee manipulation

Fifteen New Zealand White male rabbits were randomly assigned into one of two groups: control and fat embolism (FE). In FE group (n=8), the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. In the control group (n=7), a sham knee incision was made, exposing both femoral condyles, but was immediately closed without further manipulations. All animals were mechanically ventilated for an additional monitoring period of four hours post-surgical closure. For flow cytometric evaluation of platelet activation, blood samples were stained with fluorescence-conjugated antibodies against CD41 (FITC), CD62P (P-selectin) and annexin V (FITC). Platelet events were identified by their characteristic CD41 staining and size and were analyzed using a flow cytometer. All animals were mechanically ventilated for four hours post surgical closure.

The implications of platelet activation following fat embolism are numerous, ranging from adherence and aggregation, to secretion of key components of both the coagulation and inflammatory cascades.

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.

This study was undertaken to assess the contribution of pulmonary fat embolism caused by intramedullary femoral canal pressurization to the development of acute lung injury in the presence of resuscitated hemorrhagic shock. Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock and fat embolism, resuscitated hemorrhagic shock, fat embolism, and control. Fat embolism was induced via intramedullary cavity with a 1–1.5 ml bone cement injection. Only the animals that underwent resuscitated shock and fat embolism displayed amplified neutrophil activation and alveolar infiltration. 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.

The objective of this study was to assess the contribution of pulmonary 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 neutrophil activation and alveolar infiltration.

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.

CD11b mean channel florescence was only significantly elevated in the HR/FE group at two and four hours post knee manipulation. Moreover, greater infiltration of alveoli by leukocytes was only significantly higher in the HR/FE group as compared to controls.

Twenty-seven NZW rabbits were randomly assigned into one of four groups: resuscitated hemorrhagic shock + fat embolism (HR/FE), resuscitated hemorrhagic shock (HR), fat embolism (FE), and control. Hypovolemic shock was induced via carotid bleeding for one-hour prior to resuscitation. For fat embolism induction, the intramedullary cavity was drilled, reamed and pressurized with a 1–1.5 ml bone cement injection. For evaluation of neutrophil activation, blood was stained with antibodies against CD45 and CD11b and analyzed with a flow cytometer. Animals were mechanically ventilated for four hours post surgical closure. Postmortem thoracotomy was performed, and three stratified random blocks of each lung were processed for histological examination.

Our findings suggest that FE by itself does not cause lung injury, as there were no apparent differences between the control and FE animals. Only the HR/FE animals revealed a higher number of infiltrating neutrophils into alveolar spaces and greater neutrophil activation.