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In addition, the effect of <jats:styled-content style=\"fixed-case\">sEH<\/jats:styled-content> inhibitors on endothelial function was evaluated in vitro and ex vivo using isolated rat thoracic aorta.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Ischemia\u2010reperfusion (<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>) increased the myocardial damage in hearts from normal rats. <jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>\u2010induced myocardial damage was augmented in hearts isolated from hypertensive and diabetic rats. Myocardial damage as evident from increase in the activities of lactate dehydrogenase (<jats:styled-content style=\"fixed-case\">LDH<\/jats:styled-content>) and creatine kinase\u2010<jats:styled-content style=\"fixed-case\">MB<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">CK<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">MB<\/jats:styled-content>) in heart perfusate was associated with significant decrease in the heart rate and developed tension, and increase in the resting tension in isolated heart. Both <jats:styled-content style=\"fixed-case\">sEH<\/jats:styled-content> inhibitors protected the heart in normal, hypertensive, and diabetic rats subjected to <jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content> injury. The <jats:styled-content style=\"fixed-case\">sEH<\/jats:styled-content> inhibitor <jats:italic>t<\/jats:italic>\u2010<jats:styled-content style=\"fixed-case\">TUCB<\/jats:styled-content> relaxed phenylephrine precontracted aorta from normal rats. Relaxant effect of acetylcholine (<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h) was reduced in aortas from diabetic and hypertensive rats compared to normal rats. Pretreatment of <jats:styled-content style=\"fixed-case\">sEH<\/jats:styled-content> inhibitors to diabetic and hypertensive rats increased relaxant effect of <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h on aortas isolated from these rats.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Prophylactic treatment with <jats:styled-content style=\"fixed-case\">sEH<\/jats:styled-content> inhibitors decreased myocardial damage due to <jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>, hypertension and diabetes, and decreased endothelial dysfunction created by diabetes and hypertension. Therefore, inhibitors of <jats:styled-content style=\"fixed-case\">sEH<\/jats:styled-content> are useful probes to study cardiovascular pathology, and inhibition of the <jats:styled-content style=\"fixed-case\">sEH<\/jats:styled-content> is a potential approach in the management of <jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>\u2010induced cardiac damage and endothelial dysfunction\u2010related cardiovascular disorders.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1755-5922.12259","type":"journal-article","created":{"date-parts":[[2017,3,15]],"date-time":"2017-03-15T06:53:01Z","timestamp":1489560781000},"source":"Crossref","is-referenced-by-count":22,"title":["Inhibitors of soluble epoxide hydrolase minimize ischemia\u2010reperfusion\u2010induced cardiac damage in normal, hypertensive, and diabetic rats"],"prefix":"10.1111","volume":"35","author":[{"given":"Oliul","family":"Islam","sequence":"first","affiliation":[{"name":"Department of Pharmacology Al\u2010Ameen 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