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Titolo:
Na+/H+ exchange inhibition with HOE642 improves postischemic recovery due to attenuation of Ca2+ overload and prolonged acidosis on reperfusion
Autore:
Stromer, H; de Groot, MCH; Horn, M; Faul, C; Leupold, A; Morgan, JP; Scholz, W; Neubauer, S;
Indirizzi:
Univ Wurzburg, Med Klin, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 d Klin, D-97080 Wurzburg, Germany Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Cardiovasc, Boston, MA USA Harvard Univ Boston MA USA oness Med Ctr, Div Cardiovasc, Boston, MA USA HMR Deutschland GmbH, Frankfurt, Germany HMR Deutschland GmbH Frankfurt Germany schland GmbH, Frankfurt, Germany
Titolo Testata:
CIRCULATION
fascicolo: 23, volume: 101, anno: 2000,
pagine: 2749 - 2755
SICI:
0009-7322(20000613)101:23<2749:NEIWHI>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HEARTS; STUNNED MYOCARDIUM; CALCIUM OVERLOAD; FERRET HEARTS; ISCHEMIA; PROTECTION; HYPERCONTRACTURE; CARDIOMYOCYTES; CONTRACTION; AMILORIDE;
Keywords:
stunning, myocardial; myocardium; calcium; reperfusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Stromer, H Univ Wurzburg, Med Klin, Josef Schneider Str 2, D-97080 Wurzburg, Germany Univ Wurzburg Josef Schneider Str 2 Wurzburg Germany D-97080 y
Citazione:
H. Stromer et al., "Na+/H+ exchange inhibition with HOE642 improves postischemic recovery due to attenuation of Ca2+ overload and prolonged acidosis on reperfusion", CIRCULATION, 101(23), 2000, pp. 2749-2755

Abstract

Background-Na+/H+ exchange inhibition with HOE642 (cariporide) improves postischemic recovery of cardiac function, but the mechanisms of action remain speculative. Because Na+/H+ exchange is activated on reperfusion, it was hypothesized that its inhibition delays realkalinization and decreases intracellular Na+ and, via Na+/Ca2+ exchange, Ca2+ overload. Attenuated Ca2+ overload and prolonged acidosis are known to be cardioprotective. Methods and Results-Left ventricular developed and end-diastolic pressureswere measured in isolated buffer-perfused rat hearts subjected to 30 minutes of no-flow ischemia and 30 minutes of reperfusion (37 degrees C) with orwithout 1 mu mol/L HOE642 added to the perfusate 15 minutes before ischemia. Intracellular Ca2+ concentration ([Ca2+](i)) and pH(i) were measured with aequorin (n=10 per group) and P-31 NMR spectroscopy (n=6 per group), respectively. HOE642 did not affect preischemic mechanical function, [Ca2+](i),or pH(i). Mechanical recovery after 30 minutes of reperfusion was substantially improved with HOE642: left ventricular developed pressure (in percentof preischemic values) was 92+/-3 versus 49+/-7 and left ventricular end-diastolic pressure was 16+/-3 versus 46+/-5 mm Hg (P<0.05 for HOE642-\treated versus untreated hearts). End-ischemic [Ca2+](i) was significantly lower in HOE642-treated than in untreated hearts (1.04+/-0.06 versus 1.84+/-0.02 mu mol/L, P<0.05). Maximal intracellular Ca2+ overload during the first 60 seconds of reperfusion was attenuated with HOE642 compared with untreated hearts: 2.0+/-0.3 versus 3.2+/-0.3 mu mol/L (P<0.05), pH(i) was not different at end ischemia (approximate to 5.9+/-0.05). Realkalinization was similarin the first 90 seconds of reperfusion and significantly delayed in the next 3 minutes (eg, 6.8+/-0.07 in HOE642-treated hearts compared with 7.2+/-0.07 in untreated hearts; P<0.05). Conclusions-HOE642 improves postischemic recovery by reducing Ca2+ overload during ischemia and early reperfusion and by prolonging postischemic acidosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/10/20 alle ore 00:48:32