{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:12:55Z","timestamp":1791295975157,"version":"4.1.0"},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1996,1,1]]},"abstract":"<jats:p> The effects of endothelin (ET)-A (ETA)- and ETB-receptor agonist and antagonists were studied in isolated buffer-perfused rat lungs subjected to 45 min of ischemia followed by 105 min of reperfusion (I\/R). For the I\/R group after 30 and 90 min of reperfusion, the Kfc had increased three- and fivefold above control values, respectively (P &lt; 0.01), and the number of circulating neutrophils in the perfusate decreased by 65 +\/- 7.65%. Both an ETA-receptor antagonist (BQ-610) and an ETAB-receptor antagonist (PD-156707-0015) given before the ischemic period protected the lung endothelial barrier from injury associated with I\/R. Also, these compounds attenuated the I\/R-induced neutrophil accumulation in the lung (31.94 +\/- 4.16 and 34.38 +\/- 1.05%, respectively; P &lt; 0.01 compared with I\/R). Neither an ETB-receptor agonist (IRL-1620) nor an ETB-receptor antagonist (IRL-1038) affected the I\/R-induced endothelial injury. In addition, they did not alter the number of circulating polymorphonuclear cells during I\/R. ET-1 administration alone caused a dose-dependent increase in pulmonary arterial pressure, but no measurable increase in microvascular permeability occurred. We conclude that ET-1 is involved in I\/R-induced lung endothelial injury and speculate that it acts in concert with some other coactivator(s), most likely platelet-activating factor, through ETA receptors. This mechanism requires polymorphonuclear leukocyte activation with subsequent release of oxygen radicals and\/or expression of adhesive molecules on the neutrophil surface. <\/jats:p>","DOI":"10.1152\/jappl.1996.80.1.203","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T06:48:56Z","timestamp":1513925336000},"page":"203-207","source":"Crossref","is-referenced-by-count":31,"title":["Blocked ETA receptors prevent ischemia and reperfusion injury in rat lungs"],"prefix":"10.1152","volume":"80","author":[{"given":"P. L.","family":"Khimenko","sequence":"first","affiliation":[{"name":"Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. M.","family":"Moore","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. E.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","container-title":["Journal of Applied Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jappl.1996.80.1.203","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:19:58Z","timestamp":1567963198000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jappl.1996.80.1.203"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1996,1,1]]}},"alternative-id":["10.1152\/jappl.1996.80.1.203"],"URL":"https:\/\/doi.org\/10.1152\/jappl.1996.80.1.203","relation":{},"ISSN":["8750-7587","1522-1601"],"issn-type":[{"value":"8750-7587","type":"print"},{"value":"1522-1601","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,1,1]]}}}