{"doi":"10.1152/ajpheart.00855.2001","title":"Differential response to myocardial reperfusion injury  in eNOS-deficient mice","abstract":"<jats:p> Two strains of endothelial nitric oxide synthase (eNOS)-deficient (−/−) mice have been developed that respond differently to myocardial ischemia-reperfusion (MI/R). We evaluated both strains of eNOS<jats:sup>−/−</jats:sup> mice in an in vivo model of MI/R. Harvard (Har) eNOS<jats:sup>−/−</jats:sup> mice ( n = 12) experienced an 84% increase in myocardial necrosis compared with wild-type controls ( P &lt; 0.05). University of North Carolina (UNC) eNOS<jats:sup>−/−</jats:sup>( n = 10) exhibited a 52% reduction in myocardial injury versus wild-type controls ( P &lt; 0.05). PCR analysis of myocardial inducible NO synthase (iNOS) mRNA levels revealed a significant ( P &lt; 0.05) increase in the UNC eNOS<jats:sup>−/−</jats:sup> mice compared with wild-type mice, and there was no significant difference between the Har eNOS<jats:sup>−/−</jats:sup> and wild-type mice. UNC eNOS<jats:sup>−/−</jats:sup> mice treated with an iNOS inhibitor (1400W) exacerbated the extent of myocardial necrosis. When treated with 1400W, Har eNOS<jats:sup>−/−</jats:sup> did not exhibit a significant increase in myocardial necrosis. These data demonstrate that two distinct strains of eNOS<jats:sup>−/−</jats:sup> mice display opposite responses to MI/R. Although the protection seen in the UNC eNOS<jats:sup>−/−</jats:sup> mouse may result from compensatory increases in iNOS, other genes may be involved. </jats:p>","journal":"American Journal of Physiology-Heart and Circulatory Physiology","year":2002,"id":594656,"datarank":0.6830815337400812,"base_score":4.553876891600541,"endowment":4.553876891600541,"self_citation_contribution":0.6830815337400812,"citation_network_contribution":0.0,"self_endowment_contribution":0.6830815337400812,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":94,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":360821,"name":"Steven P. Jones","orcid":"0000-0001-5376-8089","position":1,"is_corresponding":false},{"id":1522393,"name":"David M. Rimmer","orcid":null,"position":2,"is_corresponding":false},{"id":465033,"name":"David J. Lefer","orcid":"0000-0003-2293-7278","position":3,"is_corresponding":false},{"id":1522389,"name":"Brent R. Sharp","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Differential response to myocardial reperfusion injury  in eNOS-deficient mice","abstract":"<jats:p> Two strains of endothelial nitric oxide synthase (eNOS)-deficient (−/−) mice have been developed that respond differently to myocardial ischemia-reperfusion (MI/R). We evaluated both strains of eNOS<jats:sup>−/−</jats:sup> mice in an in vivo model of MI/R. Harvard (Har) eNOS<jats:sup>−/−</jats:sup> mice ( n = 12) experienced an 84% increase in myocardial necrosis compared with wild-type controls ( P &lt; 0.05). University of North Carolina (UNC) eNOS<jats:sup>−/−</jats:sup>( n = 10) exhibited a 52% reduction in myocardial injury versus wild-type controls ( P &lt; 0.05). PCR analysis of myocardial inducible NO synthase (iNOS) mRNA levels revealed a significant ( P &lt; 0.05) increase in the UNC eNOS<jats:sup>−/−</jats:sup> mice compared with wild-type mice, and there was no significant difference between the Har eNOS<jats:sup>−/−</jats:sup> and wild-type mice. UNC eNOS<jats:sup>−/−</jats:sup> mice treated with an iNOS inhibitor (1400W) exacerbated the extent of myocardial necrosis. When treated with 1400W, Har eNOS<jats:sup>−/−</jats:sup> did not exhibit a significant increase in myocardial necrosis. These data demonstrate that two distinct strains of eNOS<jats:sup>−/−</jats:sup> mice display opposite responses to MI/R. Although the protection seen in the UNC eNOS<jats:sup>−/−</jats:sup> mouse may result from compensatory increases in iNOS, other genes may be involved. </jats:p>","is_dataset_classified":null,"base_score":4.553876891600541,"endowment":4.553876891600541,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"12003854","pmcid":null,"openalex_id":"https://openalex.org/W2131092630","authors":[],"funders":[{"funder_name":"NIDDK NIH HHS","grant_id":"P01-DK-43785","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"R01-HL-60849","title":null}],"total_grants":2,"fwci":3.4409,"citation_percentile":0.92781528,"influential_citations":0,"citation_trend":[{"year":2012,"count":4},{"year":2013,"count":1},{"year":2014,"count":6},{"year":2015,"count":1},{"year":2016,"count":1},{"year":2017,"count":3},{"year":2018,"count":2},{"year":2021,"count":1},{"year":2022,"count":3},{"year":2023,"count":2},{"year":2024,"count":2}],"oa_status":"closed","license":null,"oa_locations":[{"url":"https://www.physiology.org/doi/pdf/10.1152/ajpheart.00855.2001","host_type":"publisher"},{"url":"https://doi.org/10.1152/ajpheart.00855.2001","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/12003854","host_type":"repository"}],"fields_of_study":["Nitric Oxide and Endothelin Effects","Cardiac Ischemia and Reperfusion","Electron Spin Resonance Studies"],"mesh_terms":["Animals","Blood Pressure","Heart Rate","Hemodynamics","Male","Mice, Inbred C57BL","Myocardial Infarction","Myocardium","Necrosis","Proteins","RNA, Messenger","Blotting, Western","Myocardial Reperfusion Injury","Mice, Knockout","Nitric Oxide Synthase","Reverse Transcriptase Polymerase Chain Reaction","Mice","Nitric Oxide Synthase Type II","Nitric Oxide Synthase Type III"],"keywords":["Enos","Internal medicine","Endothelial nitric oxide synthase","Nitric oxide synthase","Endocrinology","Necrosis","Medicine","Nitric oxide","Reperfusion injury","Biology","Ischemia"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-07-27T15:09:30.600805Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}