Burn shock in untreated and saline-resuscitated guinea pigs development of a model

Wolfe, Robert R.; Miller, Heather G.

doi:10.1016/0022-4804(76)90037-8

Cited by 9 publications

(3 citation statements)

References 18 publications

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“…In contrast to increased β-AR activation during the ebb phase (within 48 h post-burn, where cardiac output, metabolism, and oxygen consumption are all decreased) of burn injury [ 17 , 18 , 19 , 20 ], decreased β-AR affinity has been observed in rat ventricular muscle 7 and 14 days after burn, associated with a reduced cAMP content [ 68 ]. However, another study indicated that there were no significantly changed expression levels of β-ARs (β 1 , β 2 , and β 3 ) in the rat left ventricle (LV) 7 days post-burn [ 69 ], whereas 7 days post-burn, higher β 1 -AR expression was observed in the burned right ventricle (RV) than in non-burned RV [ 69 ] This study implies burn injury-affected β-AR signaling differences between the LV and RV.…”

Section: Molecular Mechanisms Underlying Burn-impaired Cardiac Mitmentioning

confidence: 99%

“…On the other hand, myocardial contractile depression has been observed in rat hearts treated with serum from burned rats [ 16 ], suggesting that burn injury induces the production of myocardial depressant factors in systemic circulation. Importantly, the cardiac derangements can culminate in a state of shock based on animal studies [ 17 , 18 ]. Furthermore, substantial hemodynamic and cardiac dysfunction following major burn injury contribute to the development of sepsis, multiple organ failure, and death [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

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Pathological Responses of Cardiac Mitochondria to Burn Trauma

Wang

Scott

Koniaris

et al. 2020

IJMS

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Despite advances in treatment and care, burn trauma remains the fourth most common type of traumatic injury. Burn-induced cardiac failure is a key factor for patient mortality, especially during the initial post-burn period (the first 24 to 48 h). Mitochondria, among the most important subcellular organelles in cardiomyocytes, are a central player in determining the severity of myocardial damage. Defects in mitochondrial function and structure are involved in pathogenesis of numerous myocardial injuries and cardiovascular diseases. In this article, we comprehensively review the current findings on cardiac mitochondrial pathological changes and summarize burn-impaired mitochondrial respiration capacity and energy supply, induced mitochondrial oxidative stress, and increased cell death. The molecular mechanisms underlying these alterations are discussed, along with the possible influence of other biological variables. We hope this review will provide useful information to explore potential therapeutic approaches that target mitochondria for cardiac protection following burn injury.

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Section: Molecular Mechanisms Underlying Burn-impaired Cardiac Mitmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pathological Responses of Cardiac Mitochondria to Burn Trauma

Wang

Scott

Koniaris

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…Twenty-four hours after infection, the bacterial count in the untreated burns reached 2 x 10 9 CFU/g eschar. The model with slight modifications was used in the studies of prevention, 75 treatment, 74 wound healing 76 and pathogenesis 77 of infected burns as well as shock 78 and hypermetabolic response 79 induced by infected burns.…”

Section: CMmentioning

confidence: 99%