Effects of Cardioplegic Arrest and Reperfusion on Rabbit Cardiac Ryanodine Receptors

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概要

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• Calcium overload is considered to be a primary contributor to ischemia-reperfusion injury. Cardiac sarcoplasmic reticulum (SR), the main regulator of intracellular Ca^<2+> concentration under normal conditions, is a target for ischemic myocardial injury. The ryanodine receptor (RyR) is the SR Ca^<2+> 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 Ca^<2+> 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 30min of ischemia (either global ischemia (GI group) or cardioplegic arrest (CA group)), and after 20min 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±0.12pmol/mg protein, p<0.05; after reperfusion, 1.33±0.27 vs 0.80±0.08pmol/mg protein; p<0.05). CA group: after ischemia, 1.22±0.20pmol/mg protein; after reperfusion, 1.15±0.28pmol/mg protein). The affinity (Kd) values for [^3H] ryanodine binding were not different among the 3 groups at any 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.

• 社団法人日本循環器学会の論文
• 2001-03-20

著者

• Ohkusa Tomoko

  Yamaguchi University Graduate School of Medicine

• MATSUZAKI Masunori

  the Second Department of Internal Medicine, Yamaguchi University School of Medicine

• Ueyama Tsuyoshi

  Division Of Cardiology Department Of Medicine And Clinical Science Yamaguchi University Graduate Sch

• ESATO Kensuke

  the First Department of Surgery, Yamaguchi University School of Medicine

• Zempo Nobuya

  First Department Of Surgery Yamaguchi University School Of Medicine

• Esato K

  Department Of Surgery Yamaguchi University School Of Medicine

• Esato Kensuke

  First Department Of Surgery.yamaguchi University School Of Medicine

• Ueyama Takeshi

  The Second Department Of Internal Medicine Yamaguchi University School Of Medicine

• Hamano Kimikazu

  Department Of Cardiac Surgery And Clinical Sciences Yamaguchi University Graduate School Of Medicine

• OHKUSA Tomoko

  The Second Division Department of Internal Medicin,Yamaguchi University SChool Of Medicine

• Zempo Nobuya

  Department Of Surgery I Yamaguchi University School Of Medicine

• Ikeda Yoshitaka

  The First Department of Surgery

• Gohra Hidenori

  The First Department of Surgery

• Hamano Kimikazu

  The First Department of Surgery

• Zempo Nobuya

  The First Department of Surgery

• Ikeda Yoshitaka

  Department Of Surgery And Clinical Science Division Of Cardiac Surgery Yamaguchi University Graduate

• Gohra Hidenori

  Department Of Surgery Yamaguchi University School Of Medicine

• Zempo Nobuya

  First Department Of Surgery Yamaguchi University School Of Medicine.

• Esato Kensuke

  First Department Of Surgery Yamaguchi University School Of Medicine.

• Matsuzaki Masunori

  The Second Department Of Internal Medicine University Of Yamaguchi

• Zenpo Nobuya

  First Department Of Surgery Yamaguchi University School Of Medicine

• Ueyama Takeshi

  Division Of Cardiology Department Of Medicine And Clinical Science Yamaguchi University Graduate Sch

• Ohkusa Tomoko

  The Second Department Of Internal Medicine Yamaguchi University School Of Medicine

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