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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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Published in: | Wound repair and regeneration 2000-01, Vol.8 (1), p.68-76 |
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creator | Peirce, Shayn M Skalak, Thomas C Rodeheaver, George T |
description | 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. |
doi_str_mv | 10.1046/j.1524-475x.2000.00068.x |
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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. 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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.</description><subject>Animals</subject><subject>Blood Gas Monitoring, Transcutaneous</subject><subject>Chronic Disease</subject><subject>Disease Models, Animal</subject><subject>Evaluation Studies as Topic</subject><subject>Magnetics</subject><subject>Male</subject><subject>Necrosis</subject><subject>Pressure Ulcer - etiology</subject><subject>Pressure Ulcer - pathology</subject><subject>Pressure Ulcer - physiopathology</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Regional Blood Flow</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Skin - pathology</subject><subject>Skin - physiopathology</subject><issn>1067-1927</issn><issn>1524-475X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNqNkMlOwzAQhi0EgrK8AvKJW4KdxQviUpVVqkAqoPZmuc5ETUmaYieifXscUhBHDqMZab5_bH0IYUpCShJ2uQxpGiVBwtNNGBFCQl9MhJs9NPhZzPb9TBgPqIz4ETp2bumhNJXiEB1RwhmJKBug2aMzC6gKHVhYg81bV9QrXKyWrd36hs3C1qvC4LUF51oLuC0NWJzXttKNR6_wELt3D1Z1BmWXaBaArW5O0UGuSwdnu36C3u5uX0cPwfj5_nE0HAcmkVwElEeQCMIFZCJOtM4kzbgkELFYUC0SCRRi_1dJWUbmZi5kmkcUWJzrJMvnJj5BF_3dta0_WnCNqgpnoCz1CurWKU5JJIRkHhQ9aGztnIVcrW1RabtVlKjOqlqqTp7qrKrOqvq2qjY-er57o51XkP0J9ho9cN0Dn0UJ238fVtPJxA8-HvTxwjWw-Y1r-64Yj3mqpk_36kakN-N49KRe4i9QmpXV</recordid><startdate>200001</startdate><enddate>200001</enddate><creator>Peirce, Shayn M</creator><creator>Skalak, Thomas C</creator><creator>Rodeheaver, George T</creator><general>Blackwell Science Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200001</creationdate><title>Ischemia-reperfusion injury in chronic pressure ulcer formation: A skin model in the rat</title><author>Peirce, Shayn M ; Skalak, Thomas C ; Rodeheaver, George T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4978-172e48078ed834aad91d790e26381a849e1e3602916d0bcb895f21e63fa4dfbc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Blood Gas Monitoring, Transcutaneous</topic><topic>Chronic Disease</topic><topic>Disease Models, Animal</topic><topic>Evaluation Studies as Topic</topic><topic>Magnetics</topic><topic>Male</topic><topic>Necrosis</topic><topic>Pressure Ulcer - etiology</topic><topic>Pressure Ulcer - pathology</topic><topic>Pressure Ulcer - physiopathology</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Regional Blood Flow</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Skin - pathology</topic><topic>Skin - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Peirce, Shayn M</creatorcontrib><creatorcontrib>Skalak, Thomas C</creatorcontrib><creatorcontrib>Rodeheaver, George T</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Wound repair and regeneration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peirce, Shayn M</au><au>Skalak, Thomas C</au><au>Rodeheaver, George T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ischemia-reperfusion injury in chronic pressure ulcer formation: A skin model in the rat</atitle><jtitle>Wound repair and regeneration</jtitle><addtitle>Wound Repair Regen</addtitle><date>2000-01</date><risdate>2000</risdate><volume>8</volume><issue>1</issue><spage>68</spage><epage>76</epage><pages>68-76</pages><issn>1067-1927</issn><eissn>1524-475X</eissn><notes>ark:/67375/WNG-D85DL3CN-S</notes><notes>istex:F92E291521EC4A867EF106FAE1230CE43219A750</notes><notes>ArticleID:WRR068</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>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.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Inc</pub><pmid>10760216</pmid><doi>10.1046/j.1524-475x.2000.00068.x</doi><tpages>9</tpages></addata></record> |
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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 |
title | Ischemia-reperfusion injury in chronic pressure ulcer formation: A skin model in the rat |
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