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Titolo:
Successful ventricular defibrillation by the selective sodium-hydrogen exchanger isoform-1 inhibitor cariporide
Autore:
Gazmuri, RJ; Ayoub, IM; Hoffner, E; Kolarova, JD;
Indirizzi:
N Chicago VA Med Ctr, Med Serv, Sect Crit Care Med, N Chicago, IL 60064 USA N Chicago VA Med Ctr N Chicago IL USA 60064 Med, N Chicago, IL 60064 USA Finch Univ Hlth Sci Chicago Med Sch, Dept Med, Div Crit Care Med, N Chicago, IL 60064 USA Finch Univ Hlth Sci Chicago Med Sch N Chicago IL USA 60064, IL 60064 USA
Titolo Testata:
CIRCULATION
fascicolo: 2, volume: 104, anno: 2001,
pagine: 234 - 239
SICI:
0009-7322(20010710)104:2<234:SVDBTS>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
NA+-H+ EXCHANGE; CARDIOPULMONARY-RESUSCITATION; CARDIAC-ARREST; RAT-HEART; FIBRILLATION; REPERFUSION; ISCHEMIA; ARRHYTHMIAS; MYOCARDIUM; MYOCYTES;
Keywords:
cardiopulmonary resuscitation; fibrillation; ischemia; sodium-hydrogen antiporter; cariporide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Gazmuri, RJ N Chicago VA Med Ctr, Med Serv, Sect Crit Care Med, 111 F,3001Green Bay Rd, N Chicago, IL 60064 USA N Chicago VA Med Ctr 111 F,3001 Green Bay Rd N Chicago IL USA 60064
Citazione:
R.J. Gazmuri et al., "Successful ventricular defibrillation by the selective sodium-hydrogen exchanger isoform-1 inhibitor cariporide", CIRCULATION, 104(2), 2001, pp. 234-239

Abstract

Background-Sodium-hydrogen exchanger isoform-l (NHE-1)activation worsens functional myocardial abnormalities associated with ischemia and reperfusion. We hypothesize that these abnormalities may limit cardiac resuscitation from ventricular fibrillation (VF) and investigated whether NHE-1 inhibitionwith the benzoylguanidine derivative cariporide could improve resuscitability, postresuscitation myocardial function, and short-term survival in isolated heart and intact rat models of VF. Methods and Results in the isolated rat heart, VF was induced for 25 minutes. Perfusion was interrupted for the initial 10 minutes and restarted at 10% of baseline flow for the remaining 15 minutes (simulating chest compression). Cariporide ameliorated ischemic contracture, prevented postresuscitation diastolic dysfunction, and favored earlier return of contractile function. In the intact rat, cariporide, injected into the right atrium before chest compression was started (after 6 minutes of untreated VF), prompted spontaneous defibrillation between minutes 7 and 9 of chest compression in 6 of 8 rats. In contrast, electrical defibrillation was required in each of 8 control rats after completion of a predetermined 16-minute interval of VF. After resuscitation, cariporide-treated rats had less ventricular ectopic activity and normalized their hemodynamic function faster. Electrical defibrillation was then timed in control rats to match the time when spontaneous defibrillation occurred in cariporide-treated rats. With comparable VF duration, postresuscitation hemodynamic dysfunction was ameliorated by cariporide, but only when more severe ischemia was modeled by prolongation of the interval of untreated VF from 6 to 10 minutes. Conclusion-NHE-1 inhibition may represent a novel and remarkably effectiveintervention for resuscitation from VF.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/02/20 alle ore 14:14:18