Effects of dexamethasone on the contractile function of reperfused skeletal muscle

Abstract

This study evaluated the effects of dexamethasone (DXM) on contractile function of reperfused extensor digitalis longus (EDL) muscles following 3-hour ischemia and 24-hour reperfusion. The rats were divided into four groups: normal muscle, ischemia with saline treatment, ischemia/reperfusion with saline treatment, and ischemia/reperfusion with DXM treatment groups. DXM (0.6 mg kg[-1]) or saline (3.0 ml kg[-1]) was administered at 3 hours prior to ischemia. Results showed that although contractile force in all three treated groups was significantly lower than that of normal EDL, the average isometric tetanic contractile force in the DXM-treated group was significantly greater than that in the saline-treated ischemia and ischemia/reperfusion groups. A significant difference was also seen at the peak force and at 5 seconds of the fatigue trains, and with a longer fatigue half-time (FT1/2) in the DXM-treated group than in the other two groups. Histologically, edema, inflammation and necrosis of muscle fiber were less severe in the DXM-treated group than in the saline-treated group. The results indicate that pretreatment with DXM appears to attenuate, but does not completely reverse, the contractile function deficit of ischemic skeletal muscle during the first 24 hours of reperfusion.

Nitric oxide involvement in reperfusion injury of denervated muscle

“…12 The role of NO in I/R injury has been reported in a variety of tissues with varied results. We have shown the protective role of an exogenous NO donor 3,7 and relatively selective iNOS inhibitor in skeletal muscle I/R injury, 13 although a broad NOS inhibitor is detrimental. 5 Up-regulated iNOS expression also has been reported in reperfused skeletal muscle 10 and chronic hypoxic lung.…”

20(s)‑ginseonside‑Rg3 modulation of AMPK/FoxO3 signaling to attenuate mitochondrial dysfunction in a dexamethasone‑injured C2C12 myotube‑based model of skeletal atrophy in vitro

“…A growing body of evidence suggests that mitochondrial dysfunction is a key player in muscle atrophy caused by disuse and disease (47). Meanwhile, a previous study demonstrated that treatment with DEX can cause serious impairment of mitochondrial function manifesting as mitochondrial loss, dysfunctional mitochondrial respiration and disordered mitochondrial morphology and distribution (48). To counter such adverse DEX-induced effects, therapies targeting mitochondrial processes to increase mitochondrial biogenesis and/or Results were analyzed via one-way ANOVA, with data expressed as the mean ± standard deviation (n=3).…”

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

“…48,49 Glucocorticosteroids have been shown to reduce brain damage and edema, 50 to prevent neuronal degeneration after spinal cord injury 51 and compression neuropathies, 52 and to increase viability of reperfused flaps 53 and muscles. 54 Although the protective effects of steroids have been studied extensively in the central nervous system, 55 no data are available in peripheral nerve I/R injury. In this study, although MP-treated rats showed relatively earlier functional recovery compared with controls the difference was not statistically significant.…”