Trauma-Related Acute Lung Injury Develops Rapidly Irrespective of Resuscitation Strategy in the Rat

Acute lung injury (ALI) has been observed clinically after severe trauma. We have recently developed a rat model of polytrauma that shows evidence of multi-organ failure and coagulopathy. In this study, we investigate whether ALI occurs after severe trauma and resuscitation, and the cellular mechanisms involved.

Polytrauma and hemorrhage was induced in anesthetized Sprague-Dawley rats. Five groups were prepared: control, no resuscitation, and resuscitation with Lactated Ringer (LR), fresh whole blood or whole blood stored 7days at 4°C. Resuscitation was begun 1 hr after trauma. Lung injury was determined by lung wet/dry weight ratios.

Polytrauma and hemorrhage (no resuscitation) led to a significant increase in the number of neutrophils, monocytes, macrophages, platelets, and the levels of myeloperoxidase, pro-inflammatory cytokines (IL-6, IL-1α, IL-1β), anti-inflammatory Th2 cytokines (IL-4, IL-10, IL-13), and chemokines (MIP-1α, GRO KC) in the lung tissue. Resuscitation with LR, fresh whole blood or stored blood led to a significant change in the lung wet/dry ratio signifying fluid movement into the lungs. However, fluid did not move into the lungs in non-resuscitated controls.

This study shows that trauma related acute lung injury occurs early after polytrauma and hemorrhage in rat. This ALI is secondary to the trauma, and likely due to an elevation in leukocytes, platelets, inflammatory cytokines and myeloperoxidase in the lung tissue prior to any resuscitation. Resuscitation with either LR or whole blood demonstrated similar lung edema. Blood was neither more protective nor more damaging than LR during early resuscitation.