Proteasome Inhibition After Burn Injury

Vana, P. Geoff; LaPorte, Heather M.; Wong, Yee M.; Kennedy, Richard H.; Gamelli, Richard L.; Majetschak, Matthias

doi:10.1097/bcr.0000000000000280

Cited by 9 publications

(7 citation statements)

References 42 publications

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“…All aspects of a study must be fully described in order to make it reproducible. We did find two circumstances in studies that followed Walker and Mason´s model 6 ; however, the authors did not inform if they made changes to the model 13 , 14 , 19 , 20 , 23 . In reading the articles in full, we noticed changes in temperature, location and injury extent.…”

Section: Discussionmentioning

confidence: 91%

“…The sum of the water temperature and the length of exposure time to the water are important to determine the degree of the injury. Vana et al 20 . only mention ‘boiling water’, which is relative, for the boiling point of water depends on the altitude of the environment.…”

Section: Discussionmentioning

confidence: 99%

“…In order to observe a full thickness burn (third degree), 7 studies used the same amount of seconds as Walker and Mason, i.e., 10 seconds 14 , 16 , 17 , 19 , 22 , 23 , 25 . Vana et al 20 . used 16 seconds and Hoscheit et al 18 .…”

Section: Discussionmentioning

confidence: 99%

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Experimental models of scald burns. A scope review

et al. 2019

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Purpose:To conduct a scope review of the experimental model described by Walker and Mason, by identifying and analyzing the details of the method.Methods:The authors searched Pubmed-Medline, Cochrane-Bireme and PEDro databases for articles published between January 2016 and December 2018, using the following search queries: burns, burn injuries, models animal, and animal experimentation. All articles whose authors used Walker and Mason's model - with or without changes to the method in Wistar rats - were included in this study.Results:The search identified 45 mentions of Walker and Mason's model; however, after reading each summary, 20 were excluded (of which 5 due to duplicity). The inconsistencies observed after the scope review were: water temperature, length of time of exposure of the experimental model's skin to water, extent of the burnt area, and the description of the thickness/depth of the injury.Conclusions:Reproducibility of a scientific method is the basis to prove the veracity of the observed results. Thus, it is necessary to have a greater number of publications that adopt a reproducible scientific method, for this review found inconsistencies in the description of Walker and Mason's model.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Experimental models of scald burns. A scope review

et al. 2019

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“…Male Sprague Dawley rats (325–350g body weight, Harlan, Indianapolis, IN) were anesthetized with 2.5% isoflurane (Patterson Veterinary, Devens, MA), shaved, and placed into a template that exposes a dorsal body area corresponding to 30% of their total body surface area. A full thickness burn was then induced by immersion of the dorsal skin into boiling water for 17 seconds, as described previously (13,14). Sham animals were treated as described before, except that their dorsal surface was immersed in tepid water.…”

Section: Methodsmentioning

confidence: 99%

Cardiovascular Responsiveness to Vasopressin and α1-Adrenergic Receptor Agonists After Burn Injury

Evans

Vana

LaPorte

et al. 2017

Journal of Burn Care & Research

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Objective The effects of burn injury on cardiovascular responsiveness to vasoactive agents are not well understood. The aims of the present study were to determine whether burn injury alters cardiovascular reactivity to vasoactive drugs in vivo and intrinsic function of isolated mesenteric resistance arteries. Methods Anesthetized Sprague-Dawley rats were subjected to sham procedure or 30% total body surface area dorsal scald burn, followed by crystalloid resuscitation (Parkland Formula). At 24h, 72h, 96h, and 168h post-burn rats were re-anesthetized and the mean arterial blood pressure (MAP) responses to various doses of the α1-adrenergic receptor agonist phenylephrine and arginine vasopressin were tested. Mesenteric arteries were harvested from uninjured animals and at 24h and 168h post-burn. The responsiveness of arteries to phenylephrine and arginine vasopressin was tested by pressure myography. Dose response curves were generated and EC50 concentrations, Hill slopes and maximal effects were compared. Results The potency of phenylephrine to increase MAP was reduced 2-fold 24h post-burn (p<0.05 vs. sham) and gradually normalized at later time points. The reactivity of isolated arteries to phenylephrine was not significantly altered after burns. The potency of arginine vasopressin to increase MAP and to constrict isolated arteries was increased 2-3-fold at 24h post-burn (p<0.05) and normalized at later time points. Conclusions Burn injury differentially regulates vasopressor and blood pressure effects of α-adrenergic and vasopressin receptor agonists. Intrinsic vasopressin receptor reactivity of resistance arteries is sensitized early after burns. These findings will help to optimize resuscitation strategies and vasopressor use in difficult to resuscitate burn patients.

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“…Inhibition of UPS may be a therapeutic option to prevent ICUAW. Proper timing of proteasome inhibition, however, will be crucial, since its use in pre-clinical models is associated with delay and attenuation of resting energy expenditure as well as increased mortality, specifically when implemented early after injury [ 85 ].…”

Section: Mechanisms and The Potential For Intervention During And mentioning

confidence: 99%

Intensive Care Unit-Acquired Weakness: Not Just Another Muscle Atrophying Condition

Lad

Saumur

Herridge

et al. 2020

IJMS

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Intensive care unit-acquired weakness (ICUAW) occurs in critically ill patients stemming from the critical illness itself, and results in sustained disability long after the ICU stay. Weakness can be attributed to muscle wasting, impaired contractility, neuropathy, and major pathways associated with muscle protein degradation such as the ubiquitin proteasome system and dysregulated autophagy. Furthermore, it is characterized by the preferential loss of myosin, a distinct feature of the condition. While many risk factors for ICUAW have been identified, effective interventions to offset these changes remain elusive. In addition, our understanding of the mechanisms underlying the long-term, sustained weakness observed in a subset of patients after discharge is minimal. Herein, we discuss the various proposed pathways involved in the pathophysiology of ICUAW, with a focus on the mechanisms underpinning skeletal muscle wasting and impaired contractility, and the animal models used to study them. Furthermore, we will explore the contributions of inflammation, steroid use, and paralysis to the development of ICUAW and how it pertains to those with the corona virus disease of 2019 (COVID-19). We then elaborate on interventions tested as a means to offset these decrements in muscle function that occur as a result of critical illness, and we propose new strategies to explore the molecular mechanisms of ICUAW, including serum-related biomarkers and 3D human skeletal muscle culture models.

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Proteasome Inhibition After Burn Injury

Cited by 9 publications

References 42 publications

Experimental models of scald burns. A scope review

Experimental models of scald burns. A scope review

Cardiovascular Responsiveness to Vasopressin and α1-Adrenergic Receptor Agonists After Burn Injury

Intensive Care Unit-Acquired Weakness: Not Just Another Muscle Atrophying Condition

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