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Titolo:
Endothelin-1 has a unique oxygen-saving effect by increasing contractile efficiency in the isolated rat heart
Autore:
Takeuchi, Y; Kihara, Y; Inagaki, K; Yoneda, T; Sasayama, S;
Indirizzi:
Kyoto Univ, Grad Sch Med, Dept Cardiovasc Med, Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ Kyoto Japan 6068507 ovasc Med, Sakyo Ku, Kyoto 6068507, Japan
Titolo Testata:
CIRCULATION
fascicolo: 11, volume: 103, anno: 2001,
pagine: 1557 - 1563
SICI:
0009-7322(20010320)103:11<1557:EHAUOE>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYSTOLIC PRESSURE-VOLUME; VENTRICULAR MYOCYTES; ACTOMYOSIN MGATPASE; NITRIC-OXIDE; TROPONIN-I; PROTEIN; ENERGETICS; PHOSPHORYLATION; FAILURE; RESPONSIVENESS;
Keywords:
endothelin; oxygen; mechanics; contractility;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Kihara, Y Kyoto Univ, Grad Sch Med, Dept Cardiovasc Med, Sakyo Ku, 54 Shogoin Kawaharacho, Kyoto 6068507, Japan Kyoto Univ 54 Shogoin Kawaharacho Kyoto Japan 6068507 07, Japan
Citazione:
Y. Takeuchi et al., "Endothelin-1 has a unique oxygen-saving effect by increasing contractile efficiency in the isolated rat heart", CIRCULATION, 103(11), 2001, pp. 1557-1563

Abstract

Background-The effect of endothelin (ET)-1 on cardiac energetics is not fully understood. Methods and Results-In isolated, coronary-perfused rat hearts, we measuredleft ventricular contractility index (E-max), pressure-volume area (PVA), and myocardial oxygen consumption (M(V) over dot(O2)) before and after administration of ET-1 (1x10(-9) mol/L), ET-1 increased E-max by 48 +/- 16% (P<0.01) and the total M(V) over dot(O2) by 24<plus/minus>11% (P<0.01), The M(V) over dot(O2)-PVA relations were linear both before and after ET-1 (r>0.99). ET-1 shifted M(V) over dot(O2)-PVA upward, increasing the M(V) over dot(O2) intercept by 24 +/- 13%. At the same time, ET-1 decreased the slope (S), with 1/S (contractile efficiency) being 46 +/-5% before and 56 +/-5% after ET-1 (P<0.01). ET-l-induced increases in E-max and in contractile efficiency were abolished by an ETA receptor blocker (S-0139) but not by an ETB blocker (BQ-788). Although high [Ca2+] perfusion increased E-max and the intercept to the same extent as ET-1, it did not change S, N-G-Nitro-L-arginine (an inhibitor of nitric oxide synthase) increased the coronary perfusion pressure as much as ET-1, but S again remained unchanged. Dimethylamyloride(Na+/H+ exchanger inhibitor) partially blocked the positive inotropic effect of ET-1 but not the ET-l-induced increase in the contractile efficiency. Conclusions-Agonistic effects of ET-1 on the ETA receptor economized the chemomechanical conversion efficiency of the left ventricular unit myocardium by a mechanism independent of the Na+/H+ exchanger, This unique oxygen-saving effect of ET-1 may play an adaptive role in the failing myocardium, inwhich local accumulation of ET-1 is present.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/04/20 alle ore 04:16:57