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Titolo:
Transmural reentry during acute global ischemia and reperfusion in canine ventricular muscle
Autore:
Wu, JS; Zipes, DP;
Indirizzi:
Indiana Univ, Sch Med, Krannert Inst Cardiol, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 ardiol, Indianapolis, IN 46202 USA Indiana Univ, Sch Med, Dept Med, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 pt Med, Indianapolis, IN 46202 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 6, volume: 280, anno: 2001,
pagine: H2717 - H2725
SICI:
0363-6135(200106)280:6<H2717:TRDAGI>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; EXTRACELLULAR POTASSIUM; CONDUCTION-VELOCITY; CORONARY-OCCLUSION; ACTION-POTENTIALS; PORCINE HEART; ARRHYTHMIAS; MECHANISMS; ENDOCARDIUM; EPICARDIUM;
Keywords:
heart; optical mapping; arterial occlusion; tachyarrhythmias; fibrillation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Wu, JS Indiana Univ, Sch Med, Krannert Inst Cardiol, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 Indianapolis, IN 46202 USA
Citazione:
J.S. Wu e D.P. Zipes, "Transmural reentry during acute global ischemia and reperfusion in canine ventricular muscle", AM J P-HEAR, 280(6), 2001, pp. H2717-H2725

Abstract

Coronary occlusion and reperfusion produce tachyarrhythmias. We tested thehypothesis that variations in transmural activation after global ischemia and reperfusion were responsible for arrhythmias. We arterially perfused 36isolated transmural wedges from canine left ventricular free walls. After greater than or equal to 100 min of stabilization, the artery was occluded for 25 min, followed by reperfusion at various flow rates. We recorded 256 channels of fluorescent action potentials on transmural surfaces from preocclusion to >15 min after reperfusion. During endocardial pacing at 300 ms, ischemia of greater than or equal to 570 +/- 165 s (n = 34) produced 1:1 endocardial conduction and then 2:1 and 4:1 block as the wave fronts conducted toward epicardium. Transmural reentry appeared after 535 +/- 146 s of ischemia (n = 31). Further ischemia caused epicardial inactivation and eliminated reentry (n = 24). During reperfusion, tissues progressed through sequences of epicardial inactivation and reappearance of activation with 1: 1, 2:1, and 4: 1 conduction; both sustained and nonsustained reentry occurred. We conclude that heterogeneous activation responses to endocardial pacing during acute ischemia provide the substrate for initiating reentry, suppressed reentry during further ischemia, and caused reentry during reperfusion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 02:57:34