Superior Logistic Model for Decay of Ca2+ Transient and Isometric Relaxation Force Curve in Rabbit and Mouse Papillary Muscles
スポンサーリンク
概要
- 論文の詳細を見る
A decrease in myocardial intracellular calcium concentration ([Ca2+]i) precedes relaxation, and a monoexponential function is typically used for fitting the decay of the Ca2+ transient. However, a logistic function has been shown to be a better fit for the relaxation force curve, compared to the conventional monoexponential function. In the present study, we compared the logistic and monoexponential functions for fitting the [Ca2+]i declines, which were measured using the aequorin method, and isometric relaxation force curves at 4 different onsets: the minimum time-derivative of [Ca2+]i (d[Ca2+]i/dt min) and force (dF/dtmin), and the 10%, 20% and 30% lower [Ca2+]i levels and forces over the data-sampling period in 7 isolated rabbit right ventricular and 15 isolated mouse left ventricular papillary muscles. Logistic functions were significantly superior for fitting the [Ca2+] i declines and relaxation force curves, compared to monoexponential functions. Changes in the normalized logistic [Ca2+] i decline and relaxation force time constants at the delayed onsets relative to their 100% values at d[Ca2+] i/dtmin and dF/dtmin were significantly smaller than the changes in the normalized monoexponential time constants. The ratio of the logistic relaxation force time constant relative to the logistic [Ca2+]i decline time constant was significantly smaller in mouse than in rabbit. We conclude that the logistic function more reliably characterizes the [Ca2+]i decline and relaxation force curve at any onset, irrespective of animal species. Simultaneous analyses using the logistic model for decay of the Ca2+ transient and myocardial lusitropism might be a useful strategy for analysis of species-specific myocardial calcium handling.
- インターナショナル・ハート・ジャーナル刊行会の論文
著者
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YAMADA Yoshitsugu
Department of Anesthesiology, The University of Tokyo Hospital
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Kusakari Yoichiro
Department of physiology (II), The Jikei University School of Medicine
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Hirano Shuta
Department of physiology (II), The Jikei University School of Medicine
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Kurihara Satoshi
Department of physiology (II), The Jikei University School of Medicine
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Hirano Shuta
帝京大学 医学部麻酔科
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ARITA HIDEKO
Department of Anesthesiology and Pain Relief Center, The University of Tokyo Hospital
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HANAOKA KAZUO
Department of Anesthesiology and Pain Relief Center, The University of Tokyo Hospital
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Takeda Kenji
Department of Cardiology, Kanazawa Medical University
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MIZUNO Ju
Department of Anesthesiology, Faculty of Medicine, The University of Tokyo
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OTSUJI Mikiya
Department of Anesthesiology, Faculty of Medicine, The University of Tokyo
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Takeda Kenji
Department Of Cardiology Kanazawa Medical University
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Arita Hideko
Department Of Anesthesiology And Pain Relief Center The University Of Tokyo Hospital
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Hanaoka Kazuo
Department Of Anesthesia University Of Tokyo Hospital
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Otsuji Mikiya
Department Of Anesthesiology Faculty Of Medicine The University Of Tokyo
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Hirano Shuta
Department Of Cardiovascular Center Shin-katsushika Hospital
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Kurihara Satoshi
Department Of Cell Physiology The Jikei University School Of Medicine
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Yamada Yoshitsugu
Department Of Anesthesia And Pain Relief Center The University Of Tokyo Hospital
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MIZUNO Ju
Department of Anesthesiology and the Intensive Care Unit, Teikyo University School of Medicine
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Kusakari Yoichiro
Department of Cell Physiology, The Jikei University School of Medicine
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Kusakari Yoichiro
Department of Physiology, The Jikei University School of Medicine
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Hirano Shuta
Department of Physiology, The Jikei University School of Medicine
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