Abstract
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.
Correspondence should be addressed to Cynthia Vezina, Communications Manager, COA, 4150-360 Ste. Catherine St. West, Westmount, QC H3Z 2Y5, Canada
