Table 1.
Mechanism | Author(s) | Year | Animal Model | Burn Model | Conclusions |
---|---|---|---|---|---|
Autophagy | Tan et al. | 2013 | Murine | Comb model | Autophagy contributes to cell death in zone of stasis; autophagy and apoptosis peak at different time intervals |
Xiao et al. | 2013 | Murine | Heated brass rod | Induction of autophagy (with rapamycin) decreases burn wound progression and improves wound healing | |
Xiao et al. | 2014 | Murine | Heated brass rod | Autophagy is decreased and apoptosis is increased early in the course of burn progression in deep second-degree burns | |
Inflammation | Begieneman et al. | 2012 | Murine | Heated copper stamp | Long term treatment with a C1 inhibitor post-burn improves wound healing and decreases local inflammation, particularly macrophage infiltration |
Bohr et al.* | 2013 | Murine | Comb model, scald burn | Resolvin D2 prevents thrombosis of the DDVN, TNF-α secretion and secondary burn progression; Resolvin D2 does not reduce PMN infiltration | |
Eski et al. | 2011 | Murine | Comb model | Cerium nitrate baths immediately after burn injury prevent progressive tissue necrosis in the zone of stasis | |
Friedrich et al. | 2013 | Murine | Heated brass disk | TNF-α conjugated to HA more effectively prevent burn progression and decrease inflammatory markers compared to TNF-α alone or mixed with HA | |
Rizzo et al. | 2013 | Murine | Comb model | Systemic hypothermia after thermal injury decreases levels of tissue remodeling genes, increase expression of skin protective genes and reduce burn conversion | |
Singer et al.** | 2011 | Murine | Comb model | Curcumin reduces burn wound progression when administered after burn injury | |
Sun et al. | 2012 | Murine | Heated brass disk | Topical antibodies to TNF-α, but not IL-6, reduce burn wound progression | |
Ischemia | Bohr et al.† | 2013 | Murine | Scald burn | Alternative EPO-mediated signaling lessens TNF-α secretion, decreases microvascular thrombosis and reduces burn wound conversion |
Fourman et al. | 2013 | Porcine | Comb burn model | ICG angiography delineates viable versus noviable tissue in the zone of injury up to 1 hour post-burn | |
Hirth et al. | 2013 | Porcine | Heated aluminum bar | Endothelial cell necrosis at 1 hour post burn is predictive of apoptosis at 24 hours and tissue necrosis at 7 days; the zone of stasis is comprised of two vertically-divided subzones based on endothelial cell necrosis | |
Tobalem et al. | 2012 | Murine | Comb model | Early (45 minute), but not late (6 hour) EPO treatment post-burn decreases burn progression | |
Tobalem et al. | 2013 | Murine | Comb model | EPO decreases secondary burn progression in a dose-dependent manner, independent of iNOS expression, anti-inflammatory or angiogenic effects | |
Tobalem et al. | 2013 | Murine | Comb model | Immediate application of warm water to burn wounds improves early perfusion and decreases zone of stasis necrosis | |
Yuhua et al.† | 2012 | Murine | Heated brass rod | Systemic treatment with Poloxamer 188 reduces burn wound progression in deep second-degree burns | |
ROS | Deniz et al. | 2013 | Murine | Comb model | N-acetylcysteine prevents secondary tissue necrosis in the zone of stasis |
Shalom et al. | 2011 | Murine | Comb model | Prophyalactic treatment with recombinant copper-zinc SOD does not improve zone of stasis survival | |
Other | Macri et al. | 2013 | Porcine | Comb model | Immediate burn excision does not prevent burn progression in surrounding zone of stasis |
Oksuz et al. | 2013 | Murine | Comb model | Subcutaneous MSC injections 30 minutes post-burn decrease apoptosis in the zone of stasis and necrosis in the zone of stasis | |
Singer et al. | 2010 | Porcine | Comb model | Bromelain-based enzymatic debridement of burn eschar reduces tissue necrosis in the zone of stasis compared to controls | |
Singer et al. | 2013 | Murine | Comb model | Systemic MSC treatment 1 hour after burn injury reduces necrosis in the zone of stasis by around 20% | |
Turkaslan et al. | 2010 | Murine | Comb model | HBOT increases cells in the proliferative phase at 24 hours post-burn, increases tissue perfusion at 5 days post-burn, and decreases secondary necrosis in the zone of stasis |
PMN, Polymorphonuclear neutrophil; TNF-α, Tumor necrosis factor-alpha; HA, Hyaluronic acid; IL-6, Interleukin-6; ICG, Indocyanine green; EPO, Erythropoietin; iNOS, Inducible nitric oxide synthase; HBOT, Hyperbaric oxygen treatment; ROS, Reactive oxygen species; SOD, Superoxide dismutase; MSC, Mesenchymal stem cell.
Study also addressed *ischemia, **ROS, and †inflammation