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Titolo:
Depressed tolerance to fluorocarbon-simulated ischemia in failing myocardium due to impaired [Ca2+](i) modulation
Autore:
Min, JY; Hampton, TG; Wang, JF; DeAngelis, J; Morgan, JP;
Indirizzi:
Beth Israel Deaconess Med Ctr, Dept Med, Div Cardiovasc, Harvard ThorndikeLab, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr Boston MA USA 02215 b, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr, Charles A Dana Res Inst, Div Cardiovasc, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr Boston MA USA 02215 c, Boston, MA 02215 USA Harvard Univ, Sch Med, Boston, MA 02215 USA Harvard Univ Boston MA USA 02215 vard Univ, Sch Med, Boston, MA 02215 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 5, volume: 278, anno: 2000,
pagine: H1446 - H1456
SICI:
0363-6135(200005)278:5<H1446:DTTFII>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSTISCHEMIC STUNNED MYOCARDIUM; TRANSIENT CALCIUM OVERLOAD; FERRET PAPILLARY-MUSCLES; INTRACELLULAR CALCIUM; VENTRICULAR MUSCLE; CONTRACTILE FAILURE; ISOMETRIC TENSION; REPERFUSION; INTACT; RESPONSIVENESS;
Keywords:
myocardial infarction; intracellular Ca2+; contractility;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Morgan, JP Beth Israel Deaconess Med Ctr, Dept Med, Div Cardiovasc, Harvard ThorndikeLab, 330 Brookline Ave, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr 330 Brookline Ave Boston MA USA 02215
Citazione:
J.Y. Min et al., "Depressed tolerance to fluorocarbon-simulated ischemia in failing myocardium due to impaired [Ca2+](i) modulation", AM J P-HEAR, 278(5), 2000, pp. H1446-H1456

Abstract

The aim of this study was to investigate the tolerance of failing myocardium from postinfarction rats to simulated ischemia. Myocardial infarction (NI) was induced by ligation of the left coronary artery in male Wistar rats. Isometric force and free intracellular Ca2+ concentration ([Ca2+](i)) weremeasured in isolated left ventricular papillary muscles from sham-operatedand post-MI animals 6 wk after surgery. Ischemia was simulated by using fluorocarbon immersion with hypoxia. Results showed that mechanical performance was depressed during the period of hypoxia in physiological salt solution (44 +/- 7% of baseline in sham vs. 30 +/- 6% of baseline in MI, P < 0.05)or ischemia (16 +/- 2% of baseline in sham vs. 9 +/- 1% of baseline in MI,P < 0.01) accompanied by no corresponding decrease of peak [Ca2+](i) (hypoxia: 51 +/- 8% of baseline in sham vs. 46 +/- 7% of baseline in MI, P = NS;ischemia: 47 +/- 5% of baseline in sham, 39 +/- 7% of baseline in MI, P = NS). After reoxygenation, [Ca2+](i) rapidly returned to near preischemic basal levels, whereas developed tension in fluorocarbon remained significantly lower. This dissociation between peak [Ca2+](i) and isometric contractility was more pronounced in the failing myocardium from postinfarction rats. In conclusion, more severe impairment of [Ca2+](i) homeostasis in the failing myocardium from postinfarction rats increases susceptibility to ischemia-reperfusion injury.

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Documento generato il 31/03/20 alle ore 05:05:54