Modulation of the glycemic response using insulin attenuates the pulmonary response in an animal trauma model

Hyperglycemia has been shown to be an independent prognostic indicator of poor outcome in the traumatized patient. The role of insulin and the prevention of hyperglycemia in the trauma patient have as yet not been fully explored. We hypothesized that the systemic inflammatory response to trauma could be modified by modulating the glycemic response to trauma using insulin.

A rodent model of end- organ (lung) injury in trauma was chosen. Two groups underwent bilateral femur fracture and 15% blood loss. The third group was anesthetized only. The treatment group immediately received subcutaneous insulin according to a sliding scale. The control groups received normal saline subcutaneously. The animals were maintained under anesthesia for 4 hours from injury. Blood samples were then taken. Bronchoalveolar lavage was performed for neutrophil content and total protein estimation. The left lower lobe was harvested for wet:dry lung weight ratios as a measure of end-organ tissue edema.

Measures of end-organ injury, wet:dry lung weight ratios, and bronchoalveolar lavage neutrophil content were significantly reduced in the insulin-treated animals compared with in the controls (p < 0.05). Neutrophil respiratory burst activity was increased in insulin-treated animals compared with in controls (p < 0.05).

Insulin reduces leukocyte lung sequestration and end-organ (lung) edema, indicating an endothelial protective effect in this injured-animal model without attenuating neutrophil function. This work confirms that modifying the glycemic response to trauma using insulin may have a role in reducing adult respiratory distress syndrome rates in injured patients and thereby lead to improved outcomes.