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Titolo:
Effects of cardioplegic arrest and reperfusion on rabbit cardiac ryanodinereceptors
Autore:
Ikeda, Y; Gohra, H; Hamano, K; Zempo, N; Ueyama, T; Ohkusa, T; Matsuzaki, M; Esato, K;
Indirizzi:
Yamaguchi Univ, Sch Med, Dept Surg 1, Ube, Yamaguchi 7558505, Japan Yamaguchi Univ Ube Yamaguchi Japan 7558505 Ube, Yamaguchi 7558505, Japan Yamaguchi Univ, Sch Med, Dept Internal Med 2, Ube, Yamaguchi 7558505, Japan Yamaguchi Univ Ube Yamaguchi Japan 7558505 Ube, Yamaguchi 7558505, Japan
Titolo Testata:
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION
fascicolo: 4, volume: 65, anno: 2001,
pagine: 330 - 334
SICI:
0047-1828(200104)65:4<330:EOCAAR>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
SARCOPLASMIC-RETICULUM FUNCTION; DEVELOPMENTAL DIFFERENCES; MYOCARDIAL PROTECTION; RELEASE CHANNEL; CALCIUM RELEASE; GLOBAL-ISCHEMIA; CA2+ CHANNELS; MECHANISM; MG2+; ACTIVATION;
Keywords:
cardioplegia; ischemia-reperfusion injury; ryanodine receptors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Esato, K Yamaguchi Univ, Sch Med, Dept Surg 1, 1-1-1 Minamikogushi, Ube, Yamaguchi 7558505, Japan Yamaguchi Univ 1-1-1 Minamikogushi Ube Yamaguchi Japan 7558505 an
Citazione:
Y. Ikeda et al., "Effects of cardioplegic arrest and reperfusion on rabbit cardiac ryanodinereceptors", JPN CIRC J, 65(4), 2001, pp. 330-334

Abstract

Calcium overload is considered to be a primary contributor to ischemia- reperfusion injury. Cardiac sarcoplasmic reticulum (SR), the main regulator of intracellular Ca2+ concentration under normal conditions, is a target forischemic myocardial injury. The ryanodine receptor (RyR) is the SR Ca2+ release channel. previous reports have shown that a reduction in RyR activityduring global myocardial ischemia correlates with concomitant myocardial dysfunction. Crystalloid cardioplegia, a technique for myocardial protectionduring heart operations, reduces Ca2+ accumulation during global ischemia. Hence, the effects of cardioplegia on RyR in isolated rabbit hearts was investigated. The study also compared [H-3] ryanodine binding before ischemia(control group), after 30 min of ischemia (either global ischemia (GI group) or cardioplegic arrest (CA group)), and after 20 min of reperfusion. TheGI group, but not the CA group, showed a significant reduction in the maximum number of binding sites (Bmax) for RyR compared with the control group (Control vs GI group: after ischemia, 1.33 +/-0.77 vs 0.83 +/-0.12 pmol/mg protein, p<0.05; after reperfusion, 1.33<plus/minus>0.27 vs 0.80 +/-0.08pmol/mg protein; p<0.05), CA group: after ischemia, 1.3210.20pmol/mg protein; after reperfusion, 1.15<plus/minus>0.28pmol/mg protein). The affinity (Kd) values for [H-3] ryanodine binding were not different among the 3 groups atany point. The preservation of RyR numbers during cardioplegia correlated with the concomitant preservation of cardiac functions. The results indicate that number of functional RyR was much better preserved during cardioplegia than during global ischemia. It is postulated that cardioplegia-induced protection of cardiac RyR may result in the protection of SR function during ischemia- reperfusion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 12:37:43