{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,5]],"date-time":"2026-04-05T01:51:30Z","timestamp":1775353890479,"version":"3.50.1"},"reference-count":34,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2004,8,25]],"date-time":"2004-08-25T00:00:00Z","timestamp":1093392000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Anaesthesiol Scand"],"published-print":{"date-parts":[[2004,10]]},"abstract":"<jats:p><jats:bold>Background:\u2002<\/jats:bold> Sympathetic overactivity resulting from perioperative noxious stimuli elicits hyperdynamic cardiovascular responses that may lead to myocardial ischemia and\/or ventricular arrhythmia, especially in patients presenting with coronary artery disease. In the present study we investigated the cardioprotective effects of clinically relevant doses of fentanyl in an experimental model of sympathetic overactivity associated with myocardial ischemia in anesthetized rabbits.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> Central sympathetic stimulation was achieved through intracerebroventricular (i.c.v.) injection of L\u2010glutamate (10\u2003\u00b5mol), with simultaneous inhibition of nitric oxide (NO) synthesis through i.v. administration of N(omega)\u2010nitro\u2010l\u2010arginine methyl ester (L\u2010NAME; 40\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup>).<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> L\u2010glutamate triggered ventricular arrhythmia and electrocardiographic alterations indicative of myocardial ischemia. The intravenous administration of fentanyl (5, 10 or 50\u2003\u00b5g\u2003kg<jats:sup>\u22121<\/jats:sup>) reduced the incidence of ST\u2010segment shift (70, 20 and 10%, respectively, vs. 66.7% in controls) as well as of T\u2010wave inversion from 58.3% to 30, 20 and 10%, respectively. The total number of ventricular premature complexes per minute fell from 65.2\u2003\u00b1\u200316 in the control group to 6.8\u2003\u00b1\u20033, 3.5\u2003\u2003\u00b1\u2003 2 and 2.6\u2003\u00b1\u20031.5, respectively. The occurrence of ventricular tachycardia and bigeminy was completely abolished by fentanyl. Finally, the i.v. administration of fentanyl did not induce significant hemodynamic effects (except for dP\/dt<jats:sub>max<\/jats:sub> in the 50\u2003\u00b5g\u2003kg<jats:sup>\u22121<\/jats:sup>\u2010dose).<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> Fentanyl elicits significant cardioprotective effects in a model of arrhythmia resulting from the association of central sympathetic overactivity with myocardial ischemia in rabbits, independently from its systemic hemodynamic actions.<\/jats:p>","DOI":"10.1111\/j.1399-6576.2004.00472.x","type":"journal-article","created":{"date-parts":[[2004,9,7]],"date-time":"2004-09-07T12:00:07Z","timestamp":1094558407000},"page":"1115-1122","source":"Crossref","is-referenced-by-count":13,"title":["Cardioprotective action of fentanyl in a model of central sympathetic overactivity in rabbits: antiarrhythmic and anti\u2010ischemic effects"],"prefix":"10.1111","volume":"48","author":[{"given":"M. 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