Systemic effects of single hindlimb burn injury on skeletal muscle function and cyclic nucleotide levels in the murine model

Tomera, John F.; Martyn, Jeevendra

doi:10.1016/0305-4179(88)90040-x

Cited by 21 publications

(13 citation statements)

References 27 publications

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“…The left hind limb of anesthetized animals was subjected to a nonlethal scald injury, representing 3-5% total body surface area, by immersion in 90°C water for 3 s. This model (18) is considered clinically relevant to common burn injuries, as the tissue temperature between the soleus muscle and fibula reaches 46-54°C, similar to that at which human tissues show thermal damage (19). Analgesia was provided as s.c. buprenorphine at 0.05-0.1 mg͞kg, as required.…”

Section: Methodsmentioning

confidence: 99%

Burn injury causes mitochondrial dysfunction in skeletal muscle

Padfield

Astrakas

Zhang

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

100

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Severe burn trauma is generally followed by a catabolic response that leads to muscle wasting and weakness affecting skeletal musculature. Here, we perform whole-genome expression and in vivo NMR spectroscopy studies to define respectively the full set of burn-induced changes in skeletal muscle gene expression and the role of mitochondria in the altered energy expenditure exhibited by burn patients. Our results show 1,136 genes differentially expressed in a mouse hind limb burn model and identify expression pattern changes of genes involved in muscle development, protein degradation and biosynthesis, inflammation, and mitochondrial energy and metabolism. To assess further the role of mitochondria in burn injury, we performed in vivo 31 P NMR spectroscopy on hind limb skeletal muscle, to noninvasively measure high-energy phosphates and the effect of magnetization transfer on inorganic phosphate (Pi) and phosphocreatine (PCr) resonances during saturation of ␥ATP resonance, mediated by the ATP synthesis reactions. Although local burn injury does not alter high-energy phosphates or pH, apart from PCr reduction, it does significantly reduce the rate of ATP synthesis, to further implicate a role for mitochondria in burn trauma. These results, in conjunction with our genomic results showing down-regulation of mitochondrial oxidative phosphorylation and related functions, strongly suggest alterations in mitochondrial-directed energy expenditure reactions, advancing our understanding of skeletal muscle dysfunction suffered by burn injury patients. mitochondria ͉ mitochondrial oxidative phosphorylation ͉ muscle dysfunction ͉ nuclear magnetic resonance

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Section: Methodsmentioning

confidence: 99%

Burn injury causes mitochondrial dysfunction in skeletal muscle

Padfield

Astrakas

Zhang

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

100

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“…15 The hind limb model is thought to be clinically relevant for common burn injuries, as the tissue temperature between the soleus muscle and the fibula reaches 46 to 54°C, similar to that at which human tissues show thermal damage. 16 Analgesia, 0.05 to 0.1 mg/kg buprenorphine, was given subcutaneously, as required.…”

Section: Hind Limb (Local) Burn Modelmentioning

confidence: 99%

Local and Distant Burn Injury Alter Immuno-Inflammatory Gene Expression in Skeletal Muscle

Padfield

Zhang

Gopalan

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

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“…injection of 40 mg/kg pentobarbital sodium and were randomized into burn or control groups. The left hind limb of all mice in both groups (control and burn) was shaved, and each mouse in the burn group was subjected to a nonlethal scald injury of 3-5% total body surface area (TBSA) by immersion of the left hind limb in 90˚C water for 3 sec as previously described (25). The total surface area of each mouse was calculated using Meeh's formula: A = k x W 2/3 where A is the surface area in cm 2 ; k is the proportionality constant 12.3; and W is the weight in grams.…”

Section: Methodsmentioning

confidence: 99%

Murine intramyocellular lipids quantified by NMR act as metabolic biomarkers in burn trauma

Tzika

Astrakas²,

Cao³

et al. 2008

Int J Mol Med

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Abstract. It has been suggested that intramyocellular lipids (IMCLs) may serve as biomarkers of insulin resistance and mitochondrial dysfunction. Using a hind-limb mouse model of burn trauma, we tested the hypothesis that severe localized burn trauma involving 5% of the total body surface area causes a local increase in IMCLs in the leg skeletal muscle. We quantified IMCLs from ex vivo intact tissue specimens using High-Resolution Magic Angle Spinning (HRMAS) 1 H NMR and characterized the accompanying gene expression patterns in burned versus control skeletal muscle specimens. We also quantified plasma-free fatty acids (FFAs) in burn versus control mice. Our results from HRMAS 1 H NMR measurements indicated that IMCL levels were significantly increased in mice exposed to burn trauma. Furthermore, plasma FFA levels were also significantly increased, and gene expression of Glut4, insulin receptor substrate 1 (IRS1), glycolytic genes, and PGC-1ß was downregulated in these mice. Backward stepwise multiple linear regression analysis demonstrated that IMCL levels correlated significantly with FFA levels, which were a significant predictor of IRS1 and PGC-1ß gene expression. We conclude from these findings that IMCLs can serve as metabolic biomarkers in burn trauma and that FFAs and IMCLs may signal altered metabolic gene expression. This signaling may result in the observed burn-induced insulin resistance and skeletal muscle mitochondrial dysfunction.We believe that IMCLs may therefore be useful biomarkers in predicting the therapeutic effectiveness of hypolipidemic agents for patients with severe burns.

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Systemic effects of single hindlimb burn injury on skeletal muscle function and cyclic nucleotide levels in the murine model

Cited by 21 publications

References 27 publications

Burn injury causes mitochondrial dysfunction in skeletal muscle

Burn injury causes mitochondrial dysfunction in skeletal muscle

Local and Distant Burn Injury Alter Immuno-Inflammatory Gene Expression in Skeletal Muscle

Murine intramyocellular lipids quantified by NMR act as metabolic biomarkers in burn trauma

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