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Titolo:
Intracellular sodium accumulation during ischemia as the substrate for reperfusion injury
Autore:
Imahashi, K; Kusuoka, H; Hashimoto, K; Yoshioka, J; Yamaguchi, H; Nishimura, T;
Indirizzi:
Osaka Univ, Sch Med, Biomed Res Ctr, Div Tracer Kinet, Suita, Osaka 5650871, Japan Osaka Univ Suita Osaka Japan 5650871 r Kinet, Suita, Osaka 5650871, Japan
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 12, volume: 84, anno: 1999,
pagine: 1401 - 1406
SICI:
0009-7330(19990625)84:12<1401:ISADIA>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEAR-MAGNETIC-RESONANCE; PERFUSED FERRET HEARTS; NA+-H+ EXCHANGE; RAT HEARTS; CELLULAR-ENERGY; CALCIUM; OVERLOAD; NA-23; HOMEOSTASIS; INVOLVEMENT;
Keywords:
[Na+](i); Na-23 nuclear magnetic resonance spectroscopy functional recovery; time constant; low-/high-[Ca](o) reperfusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Nishimura, T Osaka Univ, Sch Med, Biomed Res Ctr, Div Tracer Kinet, D9,2-2Yamada Oka, Suita, Osaka 5650871, Japan Osaka Univ D9,2-2 Yamada Oka SuitaOsaka Japan 5650871 Japan
Citazione:
K. Imahashi et al., "Intracellular sodium accumulation during ischemia as the substrate for reperfusion injury", CIRCUL RES, 84(12), 1999, pp. 1401-1406

Abstract

To elucidate the role of intracellular Na+ kinetics during ischemia and reperfusion in postischemic contractile dysfunction, intracellular Na+ concentration ([Na+](i)) was measured in isolated perfused rat hearts using Na-23nuclear magnetic resonance spectroscopy. The extension of the ischemic period from 9 minutes to 15, 21, and 27 minutes (at 37 degrees C) increased [Na+](i) at the end of ischemia from 270.0+/-10.4% of preischemic level (mean/-SE, n=5) to 348.4+/-12.0% (n=5), 491.0+/-34.0% (n=7), and 505.3+/-12.1% (n=5), respectively, whereas the recovery of developed pressure worsened with the prolongation of the ischemic period (95.1+/-4.2%, 84.3 +/- 1.2%, 52.8 +/- 13.7%, and 16.9 +/-6.4% of preischemic level). The kinetics of [Na+](i) recovery during reperfusion was analyzed by the fitting of a monoexponential function. When the hearts were reperfused with low-[Ca](i) (0.15 mmol/L) solution, the time constants of the recovery (7) after 15-minute (8.07+/-0.85 minutes, n=5) and 21-minute ischemia (6.44+/-0.90, n 5) were significantly extended, with better functional recovery (98.5 +/- 1.4% for 15-minute [P<0.05]; 98.0+/-1.0% for 21-minute [P<0.05]) compared with standard reperfusion ([Ca],=2.0 mmol/L, tau=3.58+/-0.28 minutes for 15-minute [P<0.0001]; tau=3.02+/-0.20 for 21-minute [P<0.0001]). A selective inhibitor of Na+/Ca2+ exchanger also decelerated the [Nai]i recovery, which suggests that therecovery reflects the Na+/Ca2+ exchange activity. In contrast, high-[Ca], reperfusion (5 mmol/L) accelerated the [Na+](i) recovery after 9-minute ischemia (tau=2.48+/-0.11 minute, n=5 [P<0.0001]) and 15-minute ischemia (tau=2.10+/-0.07, n=6 [P<0.05]), but functional recovery deteriorated only in the hearts with 15-minute ischemia (29.8+/-9.4% [P<0.051]). [Nac](i) recoveryafter 27-minute ischemia was incomplete and decelerated by low-[Ca], reperfusion, with limited improvement of functional recovery (42.5+/-7.9%, n=5 [P<0.05]). These results indicate that intracellular Na+ accumulation duringischemia is the substrate for reperfusion injury and that the [Na+](i) kinetics during reperfusion, which is coupled with Ca2+ influx, also determines the degree of injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 05:03:15