Abstract
Purpose: This study determined the relative role of inflammation and ischemia in cell damage using an animal model of compartment syndrome.
Method: Forty adult Wistar rats were studied according to a protocol approved by the animal care committee at our institution. Twenty rats were used as control animals, while an additional 20 rats were pretreated with cyclophosphamide to create a leucocyte-deplete state. Animals were anesthetized using 5% isoflurane. Mean arterial pressure was maintained at 80 mm Hg and core temperature was maintained at 36 degrees. Animals were then randomly assigned to one of 4 groups, in which hindlimb compartment pressure was maintained at 30 mm Hg for 0, 15, 45, or 90 minutes. Intravital microscopy was then utilized to study capillary perfusion, white blood cell activation, and cellular damage in the hindlimb EDL muscle.
Results: Inflammation: White blood cell activation was dampened in the neutropenic animals by approximately 85 % at all time periods. Capillary Perfusion: Perfusion was similar between the neutropenic and control animals. Both groups demonstrated a gradual decrease in the number of continuously perfused capillaries, from 80 % at 0 min of elevated intracompartmental pressure (EICP) to 30 % after 90 minutes of EICP. Cellular damage: Cellular damage, measured using a differential staining technique, decreased by 55 % in the neutropenic group after 90 minutes of EICP (p< 0.005).
Conclusion: Compartment syndrome is an important clinical problem resulting in severe muscle damage. In this study, inflammation was confirmed as an important causative element of cell damage. Based upon the results of this study, adjuvant treatment to fasciotomy designed to reduce inflammation and cellular damage may have important clinical benefit.
Correspondence should be addressed to Meghan Corbeil, Meetings Coordinator Email: meghan@canorth.org