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We experimentally compared three clinically approved intravenous \u03b2-blockers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Mice undergoing 45\u2009min\/24 h ischaemia\u2013reperfusion (I\/R) received vehicle, metoprolol, atenolol, or propranolol at min 35. The effect on neutrophil infiltration was tested in three models of exacerbated inflammation. Neutrophil migration was evaluated in vitro and in vivo by intravital microscopy. The effect of \u03b2-blockers on the conformation of the \u03b21 adrenergic receptor was studied in silico. Of the tested \u03b2-blockers, only metoprolol ameliorated I\/R injury [infarct size (IS)\u2009=\u200918.0%\u2009\u00b1\u20090.03% for metoprolol vs. 35.9%\u2009\u00b1\u20090.03% for vehicle; P\u2009&amp;lt;\u20090.01]. Atenolol and propranolol had no effect on IS. In the three exacerbated inflammation models, neutrophil infiltration was significantly attenuated only in the presence of metoprolol (60%, 50%, and 70% reductions vs. vehicle in myocardial I\/R injury, thioglycolate-induced peritonitis, and lipopolysaccharide-induced acute lung injury, respectively). Migration studies confirmed the particular ability of metoprolol to disrupt neutrophil dynamics. In silico analysis indicated different intracellular \u03b21 adrenergic receptor conformational changes when bound to metoprolol than to the other two \u03b2-blockers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Metoprolol exerts a disruptive action on neutrophil dynamics during exacerbated inflammation, resulting in an infarct-limiting effect not observed with atenolol or propranolol. The differential effect of \u03b2-blockers may be related to distinct conformational changes in the \u03b21 adrenergic receptor upon metoprolol binding. If these data are confirmed in a clinical trial, metoprolol should become the intravenous \u03b2-blocker of choice for patients with ongoing infarction.<\/jats:p>\n                    <jats:p\/>\n                  <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehaa733","type":"journal-article","created":{"date-parts":[[2020,8,25]],"date-time":"2020-08-25T15:13:12Z","timestamp":1598368392000},"page":"4425-4440","source":"Crossref","is-referenced-by-count":105,"title":["Metoprolol exerts a non-class effect against ischaemia\u2013reperfusion injury by abrogating exacerbated inflammation"],"prefix":"10.1093","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3236-7822","authenticated-orcid":false,"given":"Agust\u00edn","family":"Clemente-Morag\u00f3n","sequence":"first","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M\u00f3nica","family":"G\u00f3mez","sequence":"additional","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3849-4061","authenticated-orcid":false,"given":"Roc\u00edo","family":"Villena-Guti\u00e9rrez","sequence":"additional","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dom\u00e9nica V","family":"Lalama","sequence":"additional","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaime","family":"Garc\u00eda-Prieto","sequence":"additional","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III , C\/ Monforte de Lemos 3-5. Pabell\u00f3n 11. Planta 0 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando","family":"Mart\u00ednez","sequence":"additional","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III , C\/ Monforte de Lemos 3-5. Pabell\u00f3n 11. Planta 0 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F\u00e1tima","family":"S\u00e1nchez-Cabo","sequence":"additional","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9043-9986","authenticated-orcid":false,"given":"Valent\u00edn","family":"Fuster","sequence":"additional","affiliation":[{"name":"Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), c\/Melchor Fernandez Almagro , 3. 28029 Madrid, Spain"},{"name":"Division of Cardiology, Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicina at Mount Sinai School , 1 Gustave L. 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Planta 0 28029 Madrid, Spain"},{"name":"Department of Cardiology, Instituto de Investigaci\u00f3n Sanitaria (IIS)-Fundaci\u00f3n Jim\u00e9nez D\u00edaz , Calle Isaac Peral, 42. 28015 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2020,10,7]]},"reference":[{"key":"2022102513091041900_ehaa733-B1","doi-asserted-by":"crossref","first-page":"1454","DOI":"10.1016\/j.jacc.2015.02.032","article-title":"Evolving therapies for myocardial ischemia\/reperfusion injury","volume":"65","author":"Ibanez","year":"2015","journal-title":"J Am Coll Cardiol"},{"key":"2022102513091041900_ehaa733-B2","doi-asserted-by":"crossref","first-page":"1933","DOI":"10.1016\/S0140-6736(14)60107-0","article-title":"Cardiovascular remodelling in coronary artery disease and heart 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