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Titolo:
NHE1-inhibitor cariporide prevents the transient reperfusion-induced shortening of the monophasic action potential after coronary ischemia in pigs
Autore:
Wirth, KJ; Maier, T; Busch, AE;
Indirizzi:
Aventis Pharma, DG Cardiovasc Dis, D-65926 Frankfurt, Germany Aventis Pharma Frankfurt Germany D-65926 Dis, D-65926 Frankfurt, Germany
Titolo Testata:
BASIC RESEARCH IN CARDIOLOGY
fascicolo: 2, volume: 96, anno: 2001,
pagine: 192 - 197
SICI:
0300-8428(200104)96:2<192:NCPTTR>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
NA+-H+ EXCHANGE; CARDIAC ISCHEMIA; RAT-HEART; VENTRICULAR ARRHYTHMIAS; EXTRACELLULAR POTASSIUM; MYOCARDIAL-ISCHEMIA; CALCIUM OVERLOAD; INHIBITOR; SODIUM; MYOCYTES;
Keywords:
Na+-H+-exchanger; ischemia/reperfusion; monophasic action potential duration; ventricular arrhythmias; pigs;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Wirth, KJ Aventis Pharma, DG Cardiovasc Dis, Ind Pk Hochst,H 813, D-65926 Frankfurt,Germany Aventis Pharma Ind Pk Hochst,H 813 Frankfurt Germany D-65926 ny
Citazione:
K.J. Wirth et al., "NHE1-inhibitor cariporide prevents the transient reperfusion-induced shortening of the monophasic action potential after coronary ischemia in pigs", BAS R CARD, 96(2), 2001, pp. 192-197

Abstract

During myocardial ischemia intracellular acid load increases as a consequence of anaerobic metabolism. Exchange of excessive protons for sodium via the sodium proton exchanger type 1 (NHE1) is supposed to cause intracellularsodium accumulation. The NHE1 inhibitor cariporide has been shown to inhibit ischemia and reperfusion-induced ventricular fibrillation (VF) but the mechanisms are not fully understood. During early reperfusion transient shortening of the action potential has been reported, which renders the heart susceptible to reentrant arrhythmias. In anesthetized pigs subjected to 10 min of left circumflex coronary artery (LCX) occlusion and reperfusion we have investigated whether NHE1 is involved in reperfusion-induced shortening of the monophasic action potential (MAP) taken with an epicardial probe over the ischemic area. In control pigs (n = 7) a moderate decrease in the duration of the MAP at 50 % repolarization (MAPD(50)) occurred during ischemia reaching 78.8 +/- 5.0 % of the pre-ischemic duration at 5 min (p < 0.01) and 87.3 <plus/minus>7.6 % after 10 min. An additional, transient but marked shortening occurred during the first 2 min of reperfusion, which fully recovered after 4 min. At 50 sec of reperfusion MAPD(50) fell to 53.1 + 8.2 % of the pre-ischemicvalue corresponding to 90.1 +/- 20.2 msec of reperfusion-induced shortening. Cariporide, 3 mg/kg i.v. 5 min before occlusion (n = 6), totally prevented reperfusion-induced MAP shortening while having no effect on MAPD(50) during ischemia. In conclusion, our data suggest that the immediate, transient, but strong action potential shortening during early reperfusion after 10 min of coronary ischemia is due to the activity of the NHE1.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 11:47:29