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The present review covers the physiology of skin, burn classification, burn wound pathogenesis, animal models of burn wound infection, and various topical therapeutic approaches designed to combat infection and stimulate healing.
Animal models of burn injury indicate oxygen radicals as causative agents in the local wound response, as well as in the development of burn shock and distant organ injury.
Burn patients show an impairment of ventricular compliance consistent with experimental models of burn injury [ 34- 38], and this impairment is more pronounced in the youngest patient group.
Studies in murine models of burn injury indicate that higher estrogen levels in female mice contribute to improper cell-mediated immune response to injury with an aberrant inflammatory response that increases mortality.
Insulin sensitivity has been reported to be decreased by more than 50percentt at 1-week post burn injury in pediatric patients (Cree et al. 2007) as well as in rodent models of burn injury (Carter et al. 2004).
Similar(55)
Experimental inactivation of the rhl and las systems results in marked attenuation of pseudomonal virulence in animal models of burns and pneumonia [ 36, 37].
Using a murine model of burn injury, suppression of cell-mediated immunity occurs in a gender-specific manner.
We integrated these data with a physical simulation model of burn severity informed by post-fire Landsat data.
Our findings of a hyperglycemia-induced depression of mitochondrial capacity extends previous reports on tissue respiration by Vanhorebeek in a long-term, un-resuscitated rabbit model of burn injury-induced critical illness [7, 8], inasmuch as hyperglycemia has similar effects during the acute phase of noradrenaline-resuscitated murine septic shock.
A model of burn wound healing of pig skin was applied.
In groups 5 8 we created a 'two hit' model of burn followed by sepsis.
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