PMID: 11316133Apr 24, 2001Paper

Effects of cardioplegic arrest and reperfusion on rabbit cardiac ryanodine receptors

Japanese Circulation Journal
Y IkedaK Esato

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 for ischemic myocardial injury. The ryanodine receptor (RyR) is the SR Ca2+ release channel. Previous reports have shown that a reduction in RyR activity during global myocardial ischemia correlates with concomitant myocardial dysfunction. Crystalloid cardioplegia, a technique for myocardial protection during 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 [3H] 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. The GI 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+/-0.27 vs 0.83+/-0.12 pmol/mg protein, p<0.05; after reperfusion, 1.33+/-0.27 vs 0.80+/-0.08 pmol/mg protein; p<0.05). CA group: after ischemia, 1.22+/-0.20 ...Continue Reading

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Citations

Jan 10, 2003·Circulation Journal : Official Journal of the Japanese Circulation Society·Atsushi YaoToshiyuki Takahashi
Apr 7, 2007·Journal of Cardiovascular Medicine·Naranjan S DhallaSuresh K Gupta
Mar 9, 2010·American Journal of Physiology. Heart and Circulatory Physiology·Zhen-Ying ZhangXu-Dong Wu

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