{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/86363"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/86363","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Regional Myocardial Ischemia Reperfusion Injury in Vivo: The Role of Glutathione","abstract":"201 p.","abstract_html":"201 p.","abstract_has_math":false,"creators":["Leichtweis, Steven Boyd"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Kinesiology and Community Health","degree_department":null,"school":null,"contributors":["Boileau, Richard A."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-28T15:04:17Z","date_published":"2015-09-28T15:04:17Z","updated_at":"2026-07-22T22:26:27Z","subjects":["Health Sciences, Rehabilitation and Therapy"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3070364"],"render_values":[{"text":"(MiAaPQ)AAI3070364","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/86363","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Boileau, Richard A."]},{"key":"dc:creator","label":"Author","values":["Leichtweis, Steven Boyd"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-28T15:04:17Z","10000-01-01","2002"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Kinesiology and Community Health"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Health Sciences, Rehabilitation and Therapy"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/86363","(MiAaPQ)AAI3070364"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["201 p.","The efficacy of glutathione (GSH) in protecting against ischemia-reperfusion (I-R) induced myocardial dysfunction and oxidative stress was addressed in three studies utilizing an open-chest rat model of regional, myocardial PR injury. Three major findings resulted from the first study which assessed aging, myocardial GSH status, and I-R injury. First, aged rats have a higher myocardial GSH level than adult rats. Second, during myocardial I-R the liver exports GSH into plasma, increasing the plasma GSH pool and enhancing myocardial antioxidant protection specifically at the level of the endothelial cell layer where a majority of the potential oxidants are generated. Third, adult and aged rats subjected to regional, myocardial I-R sustain similar levels of cardiovascular dysfunction and cellular oxidative damage. The second study investigated the effects of GSH depletion during myocardial I-R injury and resulted in two major findings. First, GSH deficient rats were at greater risk of cardiovascular dysfunction and oxidative damage following I-R compared to GSH adequate rats. Second, treatment by acivicin did not result in greater oxidative damage in GSH depleted rats even though these rats showed the greatest level of cardiovascular dysfunction following I-R. The third study explored the potential of GSH and other sulfhydryl compounds as potential protective supplements during I-R injury and produced two major findings. First, although sulfhydryl supplementation did not prevent cardiovascular dysfunction in rats subjected to I-R, two of the supplemented compounds prevented an increase in myocardial lipid peroxidation. Second, none of the supplemented compounds increased myocardial GSH content. Overall, the model used in these studies serves a valuable link between basic cardiovascular research on mechanisms of I-R induced cellular damage and clinical outcomes. Importantly, myocardial GSH status is not independent from the rest of the body. GSH homeostasis is a dynamic interaction between all organs and tissues. Acute myocardial I-R results in oxidative stress to the heart and a challenge to whole-body GSH homeostasis. This research provides key insights into GSH utilization during myocardial I-R injury under physiological (aging), pharmacological (depletion), and nutritional (supplementation) intervention.","Made available in DSpace on 2015-09-28T15:04:17Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 3070364.pdf: 8087218 bytes, checksum: 7f616b830038cd17527ffad0335265d7 (MD5) Previous issue date: 2002","Embargo set by: Seth Robbins for item 87644 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2002."]},{"key":"dc:title","label":"Title","values":["Regional Myocardial Ischemia Reperfusion Injury in Vivo: The Role of Glutathione"]}]}],"canonical_facts":{"dc:contributor":["Boileau, Richard A."],"dc:creator":["Leichtweis, Steven Boyd"],"dc:date":["2015-09-28T15:04:17Z","10000-01-01","2002"],"dc:description":["201 p.","The efficacy of glutathione (GSH) in protecting against ischemia-reperfusion (I-R) induced myocardial dysfunction and oxidative stress was addressed in three studies utilizing an open-chest rat model of regional, myocardial PR injury. Three major findings resulted from the first study which assessed aging, myocardial GSH status, and I-R injury. First, aged rats have a higher myocardial GSH level than adult rats. Second, during myocardial I-R the liver exports GSH into plasma, increasing the plasma GSH pool and enhancing myocardial antioxidant protection specifically at the level of the endothelial cell layer where a majority of the potential oxidants are generated. Third, adult and aged rats subjected to regional, myocardial I-R sustain similar levels of cardiovascular dysfunction and cellular oxidative damage. The second study investigated the effects of GSH depletion during myocardial I-R injury and resulted in two major findings. First, GSH deficient rats were at greater risk of cardiovascular dysfunction and oxidative damage following I-R compared to GSH adequate rats. Second, treatment by acivicin did not result in greater oxidative damage in GSH depleted rats even though these rats showed the greatest level of cardiovascular dysfunction following I-R. The third study explored the potential of GSH and other sulfhydryl compounds as potential protective supplements during I-R injury and produced two major findings. First, although sulfhydryl supplementation did not prevent cardiovascular dysfunction in rats subjected to I-R, two of the supplemented compounds prevented an increase in myocardial lipid peroxidation. Second, none of the supplemented compounds increased myocardial GSH content. Overall, the model used in these studies serves a valuable link between basic cardiovascular research on mechanisms of I-R induced cellular damage and clinical outcomes. Importantly, myocardial GSH status is not independent from the rest of the body. GSH homeostasis is a dynamic interaction between all organs and tissues. Acute myocardial I-R results in oxidative stress to the heart and a challenge to whole-body GSH homeostasis. This research provides key insights into GSH utilization during myocardial I-R injury under physiological (aging), pharmacological (depletion), and nutritional (supplementation) intervention.","Made available in DSpace on 2015-09-28T15:04:17Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 3070364.pdf: 8087218 bytes, checksum: 7f616b830038cd17527ffad0335265d7 (MD5) Previous issue date: 2002","Embargo set by: Seth Robbins for item 87644 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2002."],"dc:identifier":["http://hdl.handle.net/2142/86363","(MiAaPQ)AAI3070364"],"dc:language":["eng"],"dc:subject":["Health Sciences, Rehabilitation and Therapy"],"dc:title":["Regional Myocardial Ischemia Reperfusion Injury in Vivo: The Role of Glutathione"],"dc:type":["text"],"thesis:degree_discipline":["Kinesiology and Community Health"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:26:27Z"}