Purpose

Compartment syndrome is a limb threatening condition. Prior research has been limited by an inability to assess functional and histologic changes in muscle over time. This study was designed to assess and quantify functional deficits and histologic changes following acute compartment syndrome of the lower limb in a novel rat model.

Purpose: Recent studies have examined the systemic inflammation that occurs following spinal cord injury (SCI) (Gris et al. 2008). It is believed that this systemic inflammation plays a role in the respiratory, renal and hepatic morbidity of SCI patients, ultimately contributing to mortality post-injury. Evidence of this inflammatory response has been shown as early as two hours post SCI (Gris et al. 2008) Intravital microscopy is a powerful tool for assessing inflammation acutely and in ‘real-time’ (Brock et al. 1999). This tool would be useful for demonstrating the acuteness of a systemic inflammatory response post-SCI, and for assessing the degree of inflammation to different severities of SCI. The liver has been shown to play a particularly important role in the initiation and progression of the early systemic inflammatory response to spinal cord injury (SCI), therefore the purpose was to evaluate hepatic inflammation immediately after SCI. We hypothesized that SCI would cause immediate leukocyte recruitment and that the magnitude of inflammation would increase with increasing severity of cord injury.

Method: Male Wistar rats (200–225g) were randomly assigned to one of the following groups: uninjured, trauma-injured (laminectomy and no cord injury), cord compressed or cord transected. Spinal cord-injured rats were anesthetized by isoflurane, a dorsal laminectomy was performed, and the 4th thoracic spinal segment was injured by a moderately severe clip-compression injury or by a severe complete cord transection injury. Uninjured rats and trauma-injured rats served as controls. At 0.5 and 1.5 h after SCI rats had the left lobe of their livers externalized and visualized using intravital video microscopy.

Results: At 0.5 hours the total number of leukocytes per post-sinusoidal venule was significantly increased after cord compression and cord transection compared to that in uninjured and trauma-injured rats (P< 0.05). Of these leukocytes significantly more were either adherent or rolling along venule walls compared to uninjured and trauma-injured rats (P< 0.05). Of the rolling leukocytes 2–fold more were observed after cord transection compared to cord compression. At 1.5 h the total number of leukocytes per post-sinusoidal venule and the number of adherent leukocytes was significantly increased only after cord transection.

Conclusion: Injury to the spinal cord but not trauma alone causes immediate leukocyte recruitment to the liver within 0.5 h after injury. Also, leukocyte recruitment increases with increasing severity of injury. This is the first study to use intravital microscopy to visualize systemic inflammation in the liver following SCI.