{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T06:09:37Z","timestamp":1777529377741,"version":"3.51.4"},"reference-count":79,"publisher":"Canadian Science Publishing","issue":"9","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:p> Recently, several vasoactive molecules have been found in pericardial fluid (PF). Thus, we hypothesized that in coronary artery disease due to ischemia or ischemia\u2013reperfusion, the level of vasoconstrictors, mainly endothelin-1 (ET-1), increases in PF, which can increase the vasomotor tone of arteries. Experiments were performed using an isometric myograph. Vasomotor effects of PF from patients undergoing coronary artery bypass graft (PF<jats:sub>CABG<\/jats:sub>, n = 14) or valve replacement (PF<jats:sub>VR<\/jats:sub>, n = 7) surgery were examined in isolated rat carotid arteries (N = 14; n = 26). Vasomotor responses to KCl (40 or 60 mmol\/L) were also tested. The selective endothelin A receptor antagonist BQ123 (10<jats:sup>\u22126<\/jats:sup> mol\/L) was used to elucidate the role of ET-1. Both the first and the second additions of KCl elicited increases in the isometric force of the isolated arteries (KCl<jats:sub>1<\/jats:sub>, 6.1 \u00b1 0.2 mN; KCl<jats:sub>2<\/jats:sub>, 6.5 \u00b1 0.9 mN). PF<jats:sub>CABG<\/jats:sub> and PF<jats:sub>VR<\/jats:sub> elicited substantial increases in the isometric force of arteries (PF<jats:sub>CABG<\/jats:sub>, 3.1 \u00b1 0.7 mN; PF<jats:sub>VR<\/jats:sub>, 3.0 \u00b1 0.9 mN; p &gt; 0.05). The presence of the selective endothelin A receptor blocker significantly reduced arterial contractions to PF<jats:sub>CABG<\/jats:sub> (before BQ123, 2.6 \u00b1 0.5 mN vs. after BQ123, 0.8 \u00b1 0.1 mN; p &lt; 0.05). This study is the first to demonstrate that PFs of patients elicit substantial arterial constrictions, which is mediated primarily by ET-1. Interfering with the vasoconstrictor action of PF could be a potential therapeutic target to improve coronary blood flow in cardiac patients. <\/jats:p>","DOI":"10.1139\/cjpp-2015-0030","type":"journal-article","created":{"date-parts":[[2015,4,17]],"date-time":"2015-04-17T22:36:29Z","timestamp":1429310189000},"page":"779-785","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["Pericardial fluid of cardiac patients elicits arterial constriction: role of endothelin-1"],"prefix":"10.1139","volume":"93","author":[{"given":"Zoltan","family":"Nemeth","sequence":"first","affiliation":[{"name":"University of Pecs, Medical School, Department of Pathophysiology and Gerontology and Szentagothai Research Centre, Pecs, Hungary."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Attila","family":"Cziraki","sequence":"additional","affiliation":[{"name":"University of Pecs, Medical School, Heart Institute, Pecs, Hungary."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandor","family":"Szabados","sequence":"additional","affiliation":[{"name":"University of Pecs, Medical School, Heart Institute, Pecs, Hungary."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ivan","family":"Horvath","sequence":"additional","affiliation":[{"name":"University of Pecs, Medical School, Heart Institute, Pecs, Hungary."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akos","family":"Koller","sequence":"additional","affiliation":[{"name":"University of Pecs, Medical School, Department of Pathophysiology and Gerontology and Szentagothai Research Centre, Pecs, Hungary."},{"name":"University of Physical Education, Institute of Natural Sciences, Budapest, Hungary."},{"name":"Department of Physiology, New York Medical College, Valhalla, NY 10595, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.3317\/jraas.2002.001"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1007\/BF00304617"},{"key":"refg4\/ref4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00205.2008"},{"key":"refg5\/ref5","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2011.02.013"},{"key":"refg6\/ref6","doi-asserted-by":"publisher","DOI":"10.1016\/S0003-4975(10)65204-6"},{"key":"refg7\/ref7","doi-asserted-by":"publisher","DOI":"10.1016\/j.cardiores.2007.06.004"},{"key":"refg8\/ref8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00397.2010"},{"key":"refg9\/ref9","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1997.0470"},{"key":"refg10\/ref10","doi-asserted-by":"publisher","DOI":"10.5339\/gcsp.2014.29"},{"key":"refg11\/ref11","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-198900135-00061"},{"key":"refg12\/ref12","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.81.5.679"},{"issue":"3","key":"refg13\/ref13","first-page":"H1019","volume":"266","author":"Delyani J.A.","year":"1994","journal-title":"Am. 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