Ischemia-reperfusion injury in chronic pressure ulcer formation: A skin model in the rat

Most animal models of chronic pressure ulcers were designed to study only the role of ischemic injury in wound formation, often using single applications of constant pressure. The purpose of this study was to develop and characterize a reproducible model of cyclic ischemia‐reperfusion injury in the...

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Bibliographic Details
Published in:Wound repair and regeneration 2000-01, Vol.8 (1), p.68-76
Main Authors: Peirce, Shayn M, Skalak, Thomas C, Rodeheaver, George T
Format: Article
Language:English
Subjects:
Animals
Blood Gas Monitoring, Transcutaneous
Chronic Disease
Disease Models, Animal
Evaluation Studies as Topic
Magnetics
Male
Necrosis
Pressure Ulcer - etiology
Pressure Ulcer - pathology
Pressure Ulcer - physiopathology
Random Allocation
Rats
Rats, Sprague-Dawley
Regional Blood Flow
Reperfusion Injury - complications
Reperfusion Injury - physiopathology
Skin - pathology
Skin - physiopathology
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Summary:Most animal models of chronic pressure ulcers were designed to study only the role of ischemic injury in wound formation, often using single applications of constant pressure. The purpose of this study was to develop and characterize a reproducible model of cyclic ischemia‐reperfusion injury in the skin of small un‐anesthetized animals using clinically relevant pressures and durations. Ischemia‐reperfusion injury was created in a 9 cm2 region of dorsal skin in male rats by periodically compressing skin under a pressure of 50 mm Hg using an implanted metal plate and an overlying magnet. We varied the total number of ischemia‐reperfusion cycles, examined the effect of varying the frequency and duration of ischemic insult, and compared ischemia‐induced injury to ischemia‐reperfusion‐induced injury with this model. Tissue injury increased with an increasing number of total ischemia‐reperfusion cycles, duration of ischemia, and frequency of ischemia‐reperfusion cycles. 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 be studied and therapeutic interventions can be evaluated in a cost‐effective manner.
ISSN:1067-1927
1524-475X
DOI:10.1046/j.1524-475x.2000.00068.x