Matsen in 1975 described Compartment Syndrome (CS) as a condition in which the circulation and function of tissues within a closed space are compromised by increased pressure within that space. Raised intra-compartmental pressures result in progressive venous obstruction, capillary stagnation and microvascular hypoxia.

N-acetyl cysteine (NAC) is an anti-oxidant used clinically to reduce liver injury following paracetamol overdose. NAC has been shown previously to reduce lung injury following exposure to endotoxin. Our aim was to evaluate the efficacy of n-acetyl cysteine in the prevention of CS induced acute muscle injury.

Sprague-Dawley rats (n=6/group) were randomised into Control, CS and CS pre-treated with N-Acetyl Cysteine (0.5g/kg i.p. 1 hr prior to induction). Cremasteric muscle was isolated on its neuro-vascular pedicle and CS injury was induced by placing the muscle in a specially designed pressure chamber. Arterial blood pressure was measured via a cannula placed in the carotid artery. To induce compartment syndrome chamber pressure was maintained at diastolic-10 mm Hg. After three hours pressure was released stimulating surgical fasciotomy. One hour after decompression muscle function was assessed by electrical field stimulation: peak twitch (PTV) and maximum tetanus (MTV) values were recorded. Tissue oedema was assessed by wet to dry ratio (WDR).

Compartment Syndrome (CS) resulted in a significant decrease in muscle function (PTV, MTV). CS also resulted in a significant increase in tissue oedema (WDR). Pre-Treatment with N-Acetyl Cysteine attenuated CS injury as assessed by these parameters. These data show that administration of the anti-oxidant N-Acetyl Cysteine results in significant attenuation of the muscle injury and oedema caused by Compartment Syndrome.

This work was supported by a grant from the Cappagh Trust.

Following ischaemia-reperfusion (I-R) tissues undergo a neutrophil mediated oxidant injury. Vitamin C is a water-soluble endogenous anti-oxidant, which has been shown in previous studies to abrogate neutrophil mediated endothelial injury. Our aim was to evaluate Vitamin C supplementation in the prevention of I-R induced acute muscle injury.

Sprague-Dawley rats (n-6/group) were randomised into control, I-R and I-R pretreated with Vitamin C (3.3g over 5 days). Cremasteric muscle was isolated on its neuro-vascular pedicle and I-R injury induced by clamping the pedicle for 3 hours, the tissue was subsequently reperfused for 60 minutes. Following reperfusion muscle function was assessed by electrical field stimulation: peak twitch (PTV), maximum tetanus (MTV) and fatigability values were recorded. Tissue neutrophil infiltration was assessed by tissue myeloperoxidase (MPO) activity and tissue oedema by wet:dry ratio (WDR).

Ischaemia-reperfusion (I-R) resulted in a significant decrease in muscle function (PTV< MTV) there was no difference in fatigability values between groups. I-R also resulted in a significant increase in neutrophil infiltration (MPO) and tissue oedema (WDR). Pre-treatment with Vitamin C attenuated I-R injury as assessed by these parameters. This data suggests that oral Vitamin C reduce I-R induced acute muscle injury, possibly by attenuating neutrophil mediated tissue injury.