The Effect of Burn Wound Size on Resting Energy Expenditure

Matsuda, Takayoshi; Clark, Nicolas W.; Hariyani, G D; Bryant, Rachael; Hanumadass, Marella; Kagan, Richard J.

doi:10.1097/00005373-198702000-00002

Cited by 42 publications

(15 citation statements)

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“…Furthermore, the magnitude of the increase in REE that we observed in animals compares well with increases in REE that have been measured with indirect calorimetry in patients with similar burn sizes (33, 34). …”

Section: Discussionsupporting

confidence: 88%

“…The hallmark of the post-burn hypermetabolic response in patients is increased energy expenditure with profound protein loss. Burn-induced increases in resting energy expenditure (REE) are correlated with the degree and size of the burn injury and can reach almost 200% of normal (2, 6–8). Because skeletal muscle accounts for the majority of body cell dry weight and body protein, muscle catabolism dominates this response and is associated with increased morbidity, prolonged recovery periods and potential mortality (1, 2, 9, 10).…”

Section: Introductionmentioning

confidence: 99%

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Proteasome Inhibition After Burn Injury

Vana

LaPorte

Wong

et al. 2016

Journal of Burn Care & Research

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Objective To assess the effects of proteasome inhibition on the development of burn-induced hypermetabolism. Methods Rats underwent 30–40% TBSA scald burn or sham injury. The proteasome inhibitor bortezomib (0.1 mg/kg) or vehicle (n=10) was administered i.p. 3×weekly starting at 2h (Early-Bortezomib, n=20) or 48h (Late-Bortezomib, n=13) post-burn. Body weights were determined weekly. Resting energy expenditures (REE) were measured at days 0 (baseline), 7, 14, 21 and 42 post-burn. At day 42, blood and pectoral muscle were harvested. Routine blood chemistry parameters were analyzed. Proteasome content, proteasome peptidase activities and ubiquitin-protein conjugates were measured in muscle extracts. Results As compared with sham-vehicle treated animals, specific proteasome activities were increased after burn and vehicle treatment. Bortezomib treatment inhibited proteasome activities and increased ubiquitin-protein conjugates after sham and burn injury. Bortezomib treatment did not affect REE after sham procedure. REE significantly increased by 47% within 7 days and remained elevated until day 42 after burn and vehicle treatment. After Early-Bortezomib treatment, burn-induced increases in REE were delayed and significantly reduced by 42% at day 42, as compared with vehicle treatment. With Late-Bortezomib treatment, burn-induced increases in REE were also delayed but not attenuated at day 42. Mortality was 20% with vehicle, 65% (median survival time: 1.875 days) with Early-Bortezomib and 25% with Late-Bortezomib treatment after burns (p<0.05 Early-Bortezomib vs. vehicle and Late-Bortezomib). Conclusions Proteasome inhibition delays development of burn-induced hypermetabolism. Although proteasome inhibition early after burn injury reduces the hypermetabolic response, it significantly increases early burn-associated mortality.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Proteasome Inhibition After Burn Injury

Vana

LaPorte

Wong

et al. 2016

Journal of Burn Care & Research

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“…Depending on the degree of the burn injury, resting energy expenditure (REE) increases up to 180% of normal and can remain elevated for more than two years after injury (2, 6–8). Burn induced hypermetabolism results in muscle catabolism, which is associated with adverse outcomes and prolonged recovery periods (1, 2, 9).…”

Section: Introductionmentioning

confidence: 99%

Activities of Nonlysosomal Proteolytic Systems in Skeletal and Cardiac Muscle During Burn-Induced Hypermetabolism

Wong

Porte

Szilágyi

et al. 2014

Journal of Burn Care & Research

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Objective To assess the activity of non-lysosomal proteolytic systems in skeletal and cardiac muscle during burn induced hypermetabolism in rats. Methods Rats underwent 30% TBSA scald burn or sham injury and were observed for up to 42 days. Body weights and resting energy expenditures (REE) were determined weekly. Skeletal (soleus/pectoral) muscle and hearts were harvested on days 0 (=control), 7, 14, 21 and 42 post burn. Calpain, caspase-1, -3/7, -6, -8, -9 and proteasome peptidase activities were measured in tissue extracts. Results Hypermetabolism developed within 3 weeks after burns, as documented by increased REEs and decreased body weights on post burn days 21–42 (p<0.05 vs. control). Calpain activities did not show significant alterations. Pan caspase activities increased by time and were significantly elevated in skeletal and cardiac muscle extracts during hypermetabolism. Whereas increases in caspase-1, caspase-8 and caspase-9 activities were predominantly responsible for elevated pan caspase activities in skeletal muscle, increases in caspase-6 activities dominated in the heart. Proteasome peptidase activities in skeletal muscle extracts were not significantly altered. Proteasome peptidase activities in heart extracts increased time dependently and were significantly increased during burn induced hypermetabolism. Conclusions Activation of caspase cascades during burn induced hypermetabolism constitutes a uniform response in skeletal and cardiac muscle and may contribute to enhanced metabolic protein turnover. Activation of myocardial proteasome activities may reflect persistent cardiac stress. Further exploration of caspase cascades and the proteasome as therapeutic targets to influence long term consequences of burn induced hypermetabolism appears justified.

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“…The extent of thermal injury (%BSAB) has been suggested as a primary influencing factor by numerous investigators and, as a result, has been included in their predictive methods. 1,28,31,32,35,36,[38][39][40][41][42][43][44] The more recent publications suggest a maximum MEE of about twice that of basal. 3,35,36,38 Our data corroborate these findings as none of the patients exceeded hypermetabolism beyond 207% of predicted by the Harris Benedict equations.…”

mentioning

confidence: 99%