The influence of the C1-inhibitor BERINERT® and the protein-free haemodialysate ACTIHAEMYL20%® on the evolution of the depth of scald burns in a porcine model

Henze, U.; Lennartz, Andrea; Hafemann, B.; Goldmann, Christine; Kirkpatrick, Charles James; Klosterhalfen, B.

doi:10.1016/s0305-4179(97)00019-3

Cited by 36 publications

(28 citation statements)

References 26 publications

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“…10 Indeed, in a thermal injury model in pigs, complement inhibitor C1-inhibitor decelerated significantly the progression of the burn wound in the postburn period and prevented inflammatory tissue destruction. 11,12 In line with this, in complement factor C4 knock-out mice, burn wounds healed without contracture or scarring, whereas in burn wound healing in wild-type mice, scarring and contracture occurred. 13 Postburn blood levels of CRP were shown to be not only proportional with the extent of the burn wound area but also with the depth of the wound.…”

mentioning

confidence: 62%

“…Experiments in different animal burn models with either soluble complement receptor 1, an inhibitor of complement activation by both classical and alternative pathway, or C1 inhibitor showed that complement inhibition led to reduced neutrophil infiltration and reduced burn wound severity. [11][12][13]27 In addition to reduced tissue damage, local inhibition of inflammation may also reduce systemic complications. A recent study showed that attenuating burn wound inflammation by a locally administered p38 mitogen-activated protein kinase inhibitor improved survival in mice, 28 indicating that, indeed, attenuation of local burn wound inflammation may effect the systemic inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

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Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

Goot

Krijnen

Begieneman

et al. 2009

Journal of Burn Care & Research

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Severe burns can cause major complications, such as infection and deforming scar formation. Burn wounds induce an excessive inflammatory response. Serum levels of complement and the acute phase reactant C-reactive protein (CRP) are upregulated in response to burn injury and have been shown to be related to the severity of burn trauma and to the clinical outcome. However, complement and CRP have not been investigated on a tissue level locally at the site of the burn trauma. Protein levels and localization of complement activation product C3d and CRP were determined semi-quantitatively in burn eschar between 2 and 46 days after injury, using immunohistochemistry. CD68 and myeloperoxidase (MPO), markers for macrophages and neutrophilic granulocytes, respectively, were also analyzed on these biopsies. Skin biopsies of very recent surgical wounds (seconds old) served as controls. C3d and CRP are present at high levels in the burn wound. Protein levels of both mediators are significantly elevated up to at least 46 days after injury in comparison with control wounds. In line with this, neutrophils and macrophages infiltrate the burn wound in high numbers up to at least 46 days after injury. The excessive presence of the inflammatory mediators, complement and CRP, and the increased infiltration of neutrophils and macrophages in burn woundsup to 46 days after injury implicate a persistent ongoing acute inflammation locally in the burn wound up to weeks after the initial trauma. (J Burn Care Res 2009;30:274 -280)

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mentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

Goot

Krijnen

Begieneman

et al. 2009

Journal of Burn Care & Research

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“…The authors concluded that burn wound progression in C1 inhibitor-treated pigs was only secondary to decreased neutrophil activation and endothelial cell damage. 47 The findings of Suber et al similarly support the role of complement-induced inflammation in burn wound progression. In a mouse burn model, they found that C4Ϫ/Ϫ complement-deficient mice healed without contracture, hair loss, or neutrophil infiltration, and that complement-sufficient mice pretreated with a complement inhibitor sCR1 that blocks cleavage of C3 likewise demonstrated reduced injury postburn.…”

Section: Neutrophil Aggregation Venule Occlusion and Cytokine Produmentioning

confidence: 81%

A Review of the Local Pathophysiologic Bases of Burn Wound Progression

Shupp

Nasabzadeh

Rosenthal

et al. 2010

Journal of Burn Care & Research

194

151

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Burn wound progression refers to the phenomenon of continued tissue necrosis in the zone of stasis after abatement of the initial thermal insult. A multitude of chemical and mechanical factors contribute to the local pathophysiologic process of burn wound progression. Prolonged inflammation results in an accumulation of cytotoxic cytokines and free radicals, along with neutrophil plugging of dermal venules. Increased vascular permeability and augmentations of interstitial hydrostatic pressure lead to edema with vascular congestion. Hypercoagulability with thrombosis further impairs blood flow, while oxidative stress damages endothelial cells and compromises vascular patency. A number of studies have investigated the utility of various agents in modulating these mechanisms of burn wound progression. However, as many of studies have used animal models of burn injury, often with administration of therapy preburn, obscuring the clinical applicability of the results to burn patients is of questionable benefit. An understanding of the complex, interrelated mediators of burn wound progression and their ultimate point of convergence in effecting tissue necrosis—cell apoptosis or oncosis—will allow for the future development of therapeutic interventions.

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“…The pig burn model is basically a replicate of the rodent model except for some minor technical changes to reflect the size of the pig. Initially, the pig is sedated with intramuscular injections of Ketamine and Azaperon [68,69]. Then, the pig is put under a surgical plane and intubated by receiving pentobarbital and ketamine [68].…”

Section: Standardized Scalding Burn Model In Pigsmentioning

confidence: 99%

Animal models in burn research

Abdullahi

Amini-Nik

Jeschke

2014

Cell. Mol. Life Sci.

340

281

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Burn injury is a severe form of trauma affecting more than two million people in North America each year. Burn trauma is not a single pathophysiological event but a devastating injury that causes structural and functional deficits in numerous organ systems. Due to its complexity and the involvement of multiple organs, in vitro experiments cannot capture this complexity nor address the pathophysiology. In the past two decades, a number of burn animal models have been developed to replicate the various aspects of burn injury; to elucidate the pathophysiology and explore potential treatment interventions. Understanding the advantages and limitations of these animal models is essential for the design and development of treatments that are clinically relevant to humans. This review paper aims to highlight the common animal models of burn injury in order to provide investigators with a better understanding of the benefits and limitations of these models for translational applications. While many animal models of burn exist, we limit our discussion to the skin healing of mouse, rat, and pig. Additionally, we briefly explain hypermetabolic characteristics of burn injury and the animal model utilized to study this phenomena. Finally, we discuss the economic costs associated with each of these models in order to guide decisions of choosing the appropriate animal model for burn research.

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The influence of the C1-inhibitor BERINERT® and the protein-free haemodialysate ACTIHAEMYL20%® on the evolution of the depth of scald burns in a porcine model

Cited by 36 publications

References 26 publications

Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

Acute Inflammation is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein

A Review of the Local Pathophysiologic Bases of Burn Wound Progression

Animal models in burn research

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