{"id":{"repo_id":"uwo","oai_identifier":"oai:uwo.scholaris.ca:20.500.14721/27701"},"canonical_url":"https://search.dev.ndltd.org/etd/uwo/oai:uwo.scholaris.ca:20.500.14721/27701","repository":{"repo_id":"uwo","name":"Western University","base_url":"https://uwo.scholaris.ca/server/oai/request"},"display":{"title":"Effect of Carbon Monoxide-Releasing Molecule-3 on the Severity of Endothelial Dysfunction Due to Elevation of Hydrostatic Pressure in an In Vitro Model of Compartment Syndrome","abstract":"Compartment syndrome (CS) is a surgical emergency caused by elevated pressure within a closed osseofascial compartment. It leads to microvascular dysfunction, limiting oxygen and nutrient delivery, gas exchange, resulting in cellular anoxia, muscle necrosis and cell death. Currently, the only effective treatment is surgical fasciotomy. Recently, carbon monoxide (CO) delivered via carbon monoxide releasing molecule-3 (CORM-3) has been shown to improve microvascular perfusion and convey anti-inflammatory benefits in animal models of CS. The contribution of elevated hydrostatic pressure (EHP) to the pathophysiology of CS was examined in an in vitro model of CS. We found that EHP led to increased oxidative stress, apoptosis and structural changes within the human vascular endothelial cells; application of CORM-3 diminished the magnitude of these detrimental responses. The data suggest that CORM-3 provides beneficial effects by preventing endothelial activation while preserving endothelial integrity, making CORM-3 an excellent potential adjunct pharmacological therapeutic in CS.","abstract_html":"Compartment syndrome (CS) is a surgical emergency caused by elevated pressure within a closed osseofascial compartment. It leads to microvascular dysfunction, limiting oxygen and nutrient delivery, gas exchange, resulting in cellular anoxia, muscle necrosis and cell death. Currently, the only effective treatment is surgical fasciotomy. Recently, carbon monoxide (CO) delivered via carbon monoxide releasing molecule-3 (CORM-3) has been shown to improve microvascular perfusion and convey anti-inflammatory benefits in animal models of CS. The contribution of elevated hydrostatic pressure (EHP) to the pathophysiology of CS was examined in an in vitro model of CS. We found that EHP led to increased oxidative stress, apoptosis and structural changes within the human vascular endothelial cells; application of CORM-3 diminished the magnitude of these detrimental responses. The data suggest that CORM-3 provides beneficial effects by preventing endothelial activation while preserving endothelial integrity, making CORM-3 an excellent potential adjunct pharmacological therapeutic in CS.","abstract_has_math":false,"creators":["Taylor, Michel A."],"institution":"The University of Western Ontario","degree_name":"M Sc","degree_level":null,"degree_discipline":"Surgery","degree_department":null,"school":null,"contributors":[],"advisors":["Lawendy, Abdel-Rahman"],"committee_chairs":[],"committee_members":[],"year":2017,"date_issued":"2017-10-24","date_published":"2017-10-24","updated_at":"2026-07-27T21:55:59Z","subjects":["compartment syndrome","elevated hydrostatic pressure","human vascular endothelial cells","CORM-3","oxidative stress","apoptosis","inflammation"],"languages":["en_ca"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/20.500.14721/27701","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Lawendy, Abdel-Rahman"]},{"key":"dc:creator","label":"Author","values":["Taylor, Michel A."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2025-07-10T15:31:52Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2025-07-10T15:31:52Z"]},{"key":"dc:date.issued","label":"Date","values":["2017-10-24"]},{"key":"dc:publisher","label":"Institution","values":["The University of Western Ontario"]},{"key":"dc:type","label":"Dc Type","values":["thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Surgery"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M Sc"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["compartment syndrome","elevated hydrostatic pressure","human vascular endothelial cells","CORM-3","oxidative stress","apoptosis","inflammation"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_ca"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/20.500.14721/27701"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The thesis cover page in the PDF document includes references to Western University’s previous institutional repository platform, known as Scholarship@Western, and links to that platform (beginning with ir.lib.uwo.ca). In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."]},{"key":"dc:description.abstract","label":"Abstract","values":["Compartment syndrome (CS) is a surgical emergency caused by elevated pressure within a closed osseofascial compartment. It leads to microvascular dysfunction, limiting oxygen and nutrient delivery, gas exchange, resulting in cellular anoxia, muscle necrosis and cell death. Currently, the only effective treatment is surgical fasciotomy. Recently, carbon monoxide (CO) delivered via carbon monoxide releasing molecule-3 (CORM-3) has been shown to improve microvascular perfusion and convey anti-inflammatory benefits in animal models of CS. The contribution of elevated hydrostatic pressure (EHP) to the pathophysiology of CS was examined in an in vitro model of CS. We found that EHP led to increased oxidative stress, apoptosis and structural changes within the human vascular endothelial cells; application of CORM-3 diminished the magnitude of these detrimental responses. The data suggest that CORM-3 provides beneficial effects by preventing endothelial activation while preserving endothelial integrity, making CORM-3 an excellent potential adjunct pharmacological therapeutic in CS."]},{"key":"dc:title","label":"Title","values":["Effect of Carbon Monoxide-Releasing Molecule-3 on the Severity of Endothelial Dysfunction Due to Elevation of Hydrostatic Pressure in an In Vitro Model of Compartment Syndrome"]}]}],"canonical_facts":{"dc:contributor.advisor":["Lawendy, Abdel-Rahman"],"dc:creator":["Taylor, Michel A."],"dc:date.accessioned":["2025-07-10T15:31:52Z"],"dc:date.available":["2025-07-10T15:31:52Z"],"dc:date.issued":["2017-10-24"],"dc:description":["The thesis cover page in the PDF document includes references to Western University’s previous institutional repository platform, known as Scholarship@Western, and links to that platform (beginning with ir.lib.uwo.ca). In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."],"dc:description.abstract":["Compartment syndrome (CS) is a surgical emergency caused by elevated pressure within a closed osseofascial compartment. It leads to microvascular dysfunction, limiting oxygen and nutrient delivery, gas exchange, resulting in cellular anoxia, muscle necrosis and cell death. Currently, the only effective treatment is surgical fasciotomy. Recently, carbon monoxide (CO) delivered via carbon monoxide releasing molecule-3 (CORM-3) has been shown to improve microvascular perfusion and convey anti-inflammatory benefits in animal models of CS. The contribution of elevated hydrostatic pressure (EHP) to the pathophysiology of CS was examined in an in vitro model of CS. We found that EHP led to increased oxidative stress, apoptosis and structural changes within the human vascular endothelial cells; application of CORM-3 diminished the magnitude of these detrimental responses. The data suggest that CORM-3 provides beneficial effects by preventing endothelial activation while preserving endothelial integrity, making CORM-3 an excellent potential adjunct pharmacological therapeutic in CS."],"dc:identifier.uri":["https://hdl.handle.net/20.500.14721/27701"],"dc:language.iso":["en_ca"],"dc:publisher":["The University of Western Ontario"],"dc:subject":["compartment syndrome","elevated hydrostatic pressure","human vascular endothelial cells","CORM-3","oxidative stress","apoptosis","inflammation"],"dc:title":["Effect of Carbon Monoxide-Releasing Molecule-3 on the Severity of Endothelial Dysfunction Due to Elevation of Hydrostatic Pressure in an In Vitro Model of Compartment Syndrome"],"dc:type":["thesis"],"thesis:degree_discipline":["Surgery"],"thesis:degree_name":["M Sc"]},"updated_at":"2026-07-27T21:55:59Z"}