Compartment syndrome (CS) is a unique form of skeletal muscle ischaemia. N-acetyl cysteine (NAC) is an anti-oxidant in clinical use, with beneficial microcirculatory effects.

Sprague-Dawley rats (n=6/group) were randomised into Control, CS and CS pre-treated with NAC (0.5g/kg i.p. 1 hr prior to induction) groups. In a post-treatment group NAC was administered upon muscle decompression. Cremasteric muscle was placed in a pressure chamber in which pressure was maintained at diastolic minus 10 mm Hg for 3 hours inducing CS, muscle was then returned to the abdominal cavity. At 24 hours and 7 days post-CS contractile function was assessed by electrical stimulation. Myeloperoxidase (MPO) activity was assessed at 24-hours.

CS injury reduced twitch (50.4±7.7 vs 108.5±11.5, p<0.001; 28.1±5.5 vs. 154.7±14.1, p<0.01) and tetanic contraction (225.7±21.6 vs 455.3±23.3, p<0.001; 59.7±12.1 vs 362.9±37.2, p<0.01) compared with control at 24 hrs and 7 days respectively. NAC pre-treatment reduced CS injury at 24 hours, preserving twitch (134.3±10.4, p<0.01 vs CS) and tetanic (408.3±34.3, p<0.01 vs CS) contraction. NAC administration reduced neutrophil infiltration (MPO) at 24 hours (24.6±5.4 vs 24.6±5.4, p<0.01). NAC protection was maintained at 7 days, preserving twitch (118.2±22.9 vs 28.1±5.5, p<0.01) and tetanic contraction (256.3±37 vs 59.7±12.1, p<0.01). Administration of NAC at decompression also preserved muscle twitch (402.4±52; p<0.01 versus CS) and tetanic (402.4±52; p<0.01 versus CS) contraction, reducing neutrophil infiltration (24.6±5.4 units/g; p<0.01).

These data demonstrate NAC provided effective protection to skeletal muscle from CS induced injury when given as a pre- or post-decompression treatment.

Purpose: Compartment syndrome (CS) is a unique form of skeletal muscle ischaemia. N-acetyl cysteine (NAC) is an anti-oxidant with beneficial microcirculatory effects. We aim to assess the effect of NAC administration on CS induced muscle injury.

Methods: Sprague-Dawley rats (n=6/group) were randomised into Control, CS and CS pre-treated with NAC (0.5g/kg i.p. 1 hr prior to induction) groups. In a post-treatment group NAC was administered upon muscle decompression. Cremasteric muscle was placed in a pressure chamber in which pressure was maintained at diastolic minus 10 mm Hg for 3 hours inducing CS, muscle was then returned to the abdominal cavity. At 24 hours and 7 days post CS contractile function was assessed by electrical stimulation. Myeloperoxidase (MPO) activity were assessed at24-hours.

Results: CS injury reduced twitch (50.4 ± 7.7 vs 108.5 ± 11.5, p< 0.001; 28.1 ± 5.5 vs. 154.7 ± 14.1, p< 0.01) and tetanic contraction (225.7 ± 21.6 vs 455.3 ± 23.3, p< 0.001; 59.7 ± 12.1 vs 362.9 ± 37.2, p< 0.01) compared with control at 24hrs and 7 days respectively. NAC pre-treatment reduced CS injury at 24 hours preserving twitch (134.3 ± 10.4 , p< 0.01 vs CS) and tetanic (408.3 ± 34.3, p< 0.01 vs CS) contraction. NAC administration reduced neutrophil infiltration (MPO) at 24 hours (24.6 ± 5.4 vs 24.6 ± 5.4, p< 0.01). NAC protection was maintained at 7 days preserving twitch (118.2 ± 22.9 vs 28.1 ± 5.5, p< 0.01) and tetanic contraction (256.3 ± 37 vs 59.7 ± 12.1, p< 0.01). Administration of NAC at decompression also preserved muscle twitch (402.4 ± 52; p< 0.01 versus CS) and tetanic (402.4 ± 52; p< 0.01 versus CS) contraction, reducing neutrophil infiltration (24.6 ± 5.4 units/g; p< 0.01).

Conclusions: |NAC provides extended protection to skeletal muscle against compartment syndrome induced injury by both direct reducing neutrophil mediated tissue toxicity and by reducing neutrophil recruitment to the site of injury.