S-nitroso-n-acetylcysteine protects skeletal muscle against reperfusion injury

Abstract

The effects of a nitric oxide (NO) donor on microcirculation and contractile function of reperfused skeletal muscle were studied. Rat cremaster muscles underwent 5 hours of ischemia and 90 minutes of reperfusion and were divided into two groups systemically infused with S-nitroso-N-acetylcysteine (SNAC, 100 nmol/min) and phosphate-buffered saline (PBS), respectively. The results showed that the vessels in the SNAC group had more rapid and complete recovery than that in controls. A significant difference was found from 10 to 40 minutes and at 90 minutes in 10-20-microm arterioles, from 10 to 90 minutes in 20-40-microm arterioles, and at 10 and 90 minutes in 40-70-microm arteries. When compared to controls, SNAC-treated muscles showed larger fluorescein filling areas at 15, 30, 60, and 90 minutes and greater isometric tetanic contractile forces in response to stimulation frequencies of 40, 70, 100, and 120 Hz. The data indicate that supplementation of exogenous NO could effectively improve microcirculation and contractile function of skeletal muscle during early reperfusion.

Acute effects of N‐acetylcysteine on skeletal muscle microcirculation following closed soft tissue trauma in rats

“…However, it is also known that protective effects of NAC [8,26] and more importantly NO [9,21] depend on the local concentrations, the type of tissue (skeletal muscle), the site of production and the specific local targets. The observed beneficial effect of NAC administration and the known NAC-mediated NO-replacement in postischemic [8,26] and posttraumatic (this study) disorders suggests that compromised NO release by the dysfunctional endothelium possibly precedes and maintains ongoing microvascular and parenchymal injury, thereby initiating secondary tissue damage in CSTI. Despite neither NO nor its metabolites were measured in the present study, our results seem to indicate that microcirculatory derangements in skeletal muscle caused by CSTI represent a target which is susceptible to both, the anti-oxidant action and NO-donation by NAC.…”

N-acetylcysteine Protects Striated Muscle in a Model of Compartment Syndrome

“…Liu et al noted a similar protective effect after IRI as measured by improved arteriolar dilatation and tetanic contraction [30]. NAC also decreases muscle cell death attributable to IRI in mice as measured by malonyldialdehyde levels [8].…”

The Effects of Exogenous Nitric Oxide Donor on Motor Functional Recovery of Reperfused Peripheral Nerve

“…A walking track test was performed on days 1,7,11,14,18,21,25,28,35, and 42 of reperfusion in all rats. The procedure followed our previously established protocol.…”