{"id":{"repo_id":"vcu","oai_identifier":"oai:scholarscompass.vcu.edu:etd-2363"},"canonical_url":"https://search.dev.ndltd.org/etd/vcu/oai:scholarscompass.vcu.edu:etd-2363","repository":{"repo_id":"vcu","name":"Virginia Commonwealth University","base_url":"https://scholarscompass.vcu.edu/do/oai/"},"display":{"title":"Early Mediators of Cutaneous Ischemia Reperfusion Injury: A Mouse Model","abstract":"Chronic tissue injuries present an enormous problem to both patients and healthcare professionals, and yet little is definitively known as to the underlying pathophysiology. While there are numerous comorbidities associated with these wounds, a unifying theme has been proposed to be the repetitive incidence of ischemia reperfusion injury.A mouse model of cyclic ischemia reperfusion was employed to examine the initiation events in the pathology of chronic wounds. Mice were subjected to eight hours of magnetic skin compression via four cycles of two-hours ischemia and thirty minutes of reperfusion. The presence of neutrophil markers of oxidative stress and inflammation such as myeloperoxidase and matrix metalloproteinases were measured at time points 1, 3, & 5 days post-injury. A sharp increase in MPO and MMP-9 was witnessed throughout, with the highest concentrations found at day 1. Simultaneously, immunodetection of heme oxygenase was performed, revealing high levels of inducible HO-I throughout the time course, with no change in HO-2 expression. Tissue damage was confirmed through histological examination.","abstract_html":"Chronic tissue injuries present an enormous problem to both patients and healthcare professionals, and yet little is definitively known as to the underlying pathophysiology. While there are numerous comorbidities associated with these wounds, a unifying theme has been proposed to be the repetitive incidence of ischemia reperfusion injury.A mouse model of cyclic ischemia reperfusion was employed to examine the initiation events in the pathology of chronic wounds. Mice were subjected to eight hours of magnetic skin compression via four cycles of two-hours ischemia and thirty minutes of reperfusion. The presence of neutrophil markers of oxidative stress and inflammation such as myeloperoxidase and matrix metalloproteinases were measured at time points 1, 3, & 5 days post-injury. A sharp increase in MPO and MMP-9 was witnessed throughout, with the highest concentrations found at day 1. Simultaneously, immunodetection of heme oxygenase was performed, revealing high levels of inducible HO-I throughout the time course, with no change in HO-2 expression. Tissue damage was confirmed through histological examination.","abstract_has_math":false,"creators":["Pruitt, Christopher Rogers"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Physiology","degree_department":null,"school":null,"contributors":["Dr. Dorne R. Yager"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2006,"date_issued":"2006-01-01T08:00:00Z","date_published":"2006-01-01T08:00:00Z","updated_at":"2026-07-24T05:55:14Z","subjects":["pressure ulcer","tissue injury","Life Sciences","Physiology"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/1364"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/1364","href":"https://scholarscompass.vcu.edu/etd/1364","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/JJ3R-YB33","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Dr. Dorne R. 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While there are numerous comorbidities associated with these wounds, a unifying theme has been proposed to be the repetitive incidence of ischemia reperfusion injury.A mouse model of cyclic ischemia reperfusion was employed to examine the initiation events in the pathology of chronic wounds. Mice were subjected to eight hours of magnetic skin compression via four cycles of two-hours ischemia and thirty minutes of reperfusion. The presence of neutrophil markers of oxidative stress and inflammation such as myeloperoxidase and matrix metalloproteinases were measured at time points 1, 3, & 5 days post-injury. A sharp increase in MPO and MMP-9 was witnessed throughout, with the highest concentrations found at day 1. Simultaneously, immunodetection of heme oxygenase was performed, revealing high levels of inducible HO-I throughout the time course, with no change in HO-2 expression. Tissue damage was confirmed through histological examination."]},{"key":"dc:title","label":"Title","values":["Early Mediators of Cutaneous Ischemia Reperfusion Injury: A Mouse Model"]}]}],"canonical_facts":{"dc:contributor":["Dr. Dorne R. Yager"],"dc:creator":["Pruitt, Christopher Rogers"],"dc:date.available":["2014-07-09T07:00:00Z"],"dc:description.abstract":["Chronic tissue injuries present an enormous problem to both patients and healthcare professionals, and yet little is definitively known as to the underlying pathophysiology. While there are numerous comorbidities associated with these wounds, a unifying theme has been proposed to be the repetitive incidence of ischemia reperfusion injury.A mouse model of cyclic ischemia reperfusion was employed to examine the initiation events in the pathology of chronic wounds. Mice were subjected to eight hours of magnetic skin compression via four cycles of two-hours ischemia and thirty minutes of reperfusion. The presence of neutrophil markers of oxidative stress and inflammation such as myeloperoxidase and matrix metalloproteinases were measured at time points 1, 3, & 5 days post-injury. A sharp increase in MPO and MMP-9 was witnessed throughout, with the highest concentrations found at day 1. Simultaneously, immunodetection of heme oxygenase was performed, revealing high levels of inducible HO-I throughout the time course, with no change in HO-2 expression. Tissue damage was confirmed through histological examination."],"dc:identifier":["https://doi.org/10.25772/JJ3R-YB33","https://scholarscompass.vcu.edu/etd/1364"],"dc:rights":["© The Author"],"dc:subject":["pressure ulcer","tissue injury","Life Sciences","Physiology"],"dc:title":["Early Mediators of Cutaneous Ischemia Reperfusion Injury: A Mouse Model"],"thesis:degree_discipline":["Physiology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T05:55:14Z"}