Most animal models of chronic pressure ulcers were designed to study only t
he role of ischemic injury in wound formation, often using single applicati
ons of constant pressure. The purpose of this study was to develop and char
acterize a reproducible model of cyclic ischemia-reperfusion injury in the
skin of small un-anesthetized animals using clinically relevant pressures a
nd durations. Ischemia-reperfusion injury was created in a 9 cm(2) region o
f dorsal skin in male rats by periodically compressing skin under a pressur
e of 50 mm Hg using an implanted metal plate and an overlying magnet. We va
ried the total number of ischemia-reperfusion cycles, examined the effect o
f varying the frequency and duration of ischemic insult, and compared ische
mia-induced injury to ischemia-reperfusion-induced injury with this model.
Tissue injury increased with an increasing number of total ischemia-reperfu
sion cycles, duration of ischemia, and frequency of ischemia-reperfusion cy
cles. This model generates reproducible ischemia-reperfusion skin injury as
characterized by tissue necrosis, wound thickness, leukocyte infiltration,
transcutaneous oxygen tension, and wound blood flow, Using this model, the
biological markers of ischemia-reperfusion-induced wound development can b
e studied and therapeutic interventions can be evaluated in a cost-effectiv
e manner.