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The beneficial effects of H2S appear to be mediated through endothelial nitric oxide-dependent pathways.","abstract_has_math":false,"creators":["Jensen, Amanda"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Markel, Troy"],"committee_chairs":[],"committee_members":[],"year":2017,"date_issued":"2017","date_published":"2017","updated_at":"2026-08-21T22:21:56Z","subjects":["H2S","eNOS","Intestinal ischemia"],"languages":["en_US"],"rights":["Attribution-NonCommercial-NoDerivs 3.0 United States"],"rights_urls":["http://creativecommons.org/licenses/by-nc-nd/3.0/us/"],"identifier_entries":[{"key":"dc:identifier.doi","label":"DOI","values":["10.7912/C2PH2K"],"render_values":[{"text":"10.7912/C2PH2K","href":"https://doi.org/10.7912/C2PH2K","code":true}]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://dx.doi.org/10.7912/C2/2774"],"render_values":[{"text":"http://dx.doi.org/10.7912/C2/2774","href":"http://dx.doi.org/10.7912/C2/2774","code":true}]}]},"links":{"outbound_url":"https://hdl.handle.net/1805/17057","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"source_record":{"url":"https://scholarworks.indianapolis.iu.edu/server/oai/request?verb=GetRecord&metadataPrefix=dim&identifier=oai%3Ascholarworks.indianapolis.iu.edu%3A1805%2F17057","prefix":"dim"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Markel, Troy"]},{"key":"dc:creator","label":"Author","values":["Jensen, Amanda"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2018-08-09T19:14:32Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2018-08-09T19:14:32Z"]},{"key":"dc:date.issued","label":"Date","values":["2017"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["H2S","eNOS","Intestinal ischemia"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_US"]},{"key":"dc:rights","label":"Dc Rights","values":["Attribution-NonCommercial-NoDerivs 3.0 United States"]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://creativecommons.org/licenses/by-nc-nd/3.0/us/"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.doi","label":"DOI","values":["10.7912/C2PH2K"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/1805/17057","http://dx.doi.org/10.7912/C2/2774"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Indiana University Purdue University Indianapolis"]},{"key":"dc:description.abstract","label":"Abstract","values":["H2S is a gaseous mediator that acts as an anti-inflammatory agent contributing to gastrointestinal mucosal defense. It promotes vascular dilation, mucosal repair, and resolution of inflammation following intestinal ischemia and may be exploited as a novel therapeutic agent. It is unclear if H2S works through nitric oxide-dependent pathways in the intestine. We appreciated that H2S was able to improve post-ischemic recovery of mesenteric perfusion, mucosal integrity, and inflammation. The beneficial effects of H2S appear to be mediated through endothelial nitric oxide-dependent pathways."]},{"key":"dc:title","label":"Title","values":["Hydrogen sulfide therapy improves intestinal recovery through endothelial nitric oxide dependent mechanisms"]}]}],"canonical_facts":{"dc:contributor.advisor":["Markel, Troy"],"dc:creator":["Jensen, Amanda"],"dc:date.accessioned":["2018-08-09T19:14:32Z"],"dc:date.available":["2018-08-09T19:14:32Z"],"dc:date.issued":["2017"],"dc:description":["Indiana University Purdue University Indianapolis"],"dc:description.abstract":["H2S is a gaseous mediator that acts as an anti-inflammatory agent contributing to gastrointestinal mucosal defense. It promotes vascular dilation, mucosal repair, and resolution of inflammation following intestinal ischemia and may be exploited as a novel therapeutic agent. It is unclear if H2S works through nitric oxide-dependent pathways in the intestine. We appreciated that H2S was able to improve post-ischemic recovery of mesenteric perfusion, mucosal integrity, and inflammation. The beneficial effects of H2S appear to be mediated through endothelial nitric oxide-dependent pathways."],"dc:identifier.doi":["10.7912/C2PH2K"],"dc:identifier.uri":["https://hdl.handle.net/1805/17057","http://dx.doi.org/10.7912/C2/2774"],"dc:language.iso":["en_US"],"dc:rights":["Attribution-NonCommercial-NoDerivs 3.0 United States"],"dc:rights.uri":["http://creativecommons.org/licenses/by-nc-nd/3.0/us/"],"dc:subject":["H2S","eNOS","Intestinal ischemia"],"dc:title":["Hydrogen sulfide therapy improves intestinal recovery through endothelial nitric oxide dependent mechanisms"]},"updated_at":"2026-08-21T22:21:56Z"}