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Cardiovascular Research 2001 51(1):122-130; doi:10.1016/S0008-6363(01)00277-2
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Oxygen wastage of stunned myocardium in vivo is due to an increased oxygen cost of contractility and a decreased myofibrillar efficiency

Serge A.I.P. Trinesa, Cornelis J. Slagera, Tessa A.M. Onderwatera, Jos M.J. Lamersb, Pieter D. Verdouwa and Rob Kramsa,*

aDepartment of Cardiology, Thoraxcentre, Erasmus Medical Centre Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands
bDepartment of Biochemistry, Erasmus Medical Centre Rotterdam, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands

* Corresponding author. Tel.: +31-10-408-8029; fax: +31-10-408-9494 krams{at}tch.fgg.eur.nl

Objective: We investigated whether an increased oxygen cost of contractility and/or a decreased myofibrillar efficiency contribute to oxygen wastage of stunned myocardium. Because Ca2+-sensitizers may increase myofibrillar Ca2+-sensitivity without increasing cross-bridge cycling, we also investigated whether EMD 60263 restores myofibrillar efficiency and/or the oxygen cost of contractility. Methods: Regional fiber stress and strain were calculated from mesomyocardially implanted ultrasound crystals and left ventricular pressure in anesthetized pigs (n=18). Regional myocardial oxygen consumption (MVO2) was measured before contractility (end-systolic elastance, Ees) and total myofibrillar work (stress–strain area, SSA) were determined from stress–strain relationships. Atrial pacing at three heart rates and two doses of dobutamine were used to vary SSA and Ees, respectively. After stunning (two times 10-min ischemia followed by 30-min reperfusion), measurements were repeated following infusion of saline (n=8) or EMD 60263 (1.5 mg·kg–1 i.v., n=10). Linear regression was performed using: MVO2={alpha}·SSA+β·Ees+{gamma}·HR–1 ({alpha}–1, myofibrillar efficiency; β, oxygen cost of contractility; and {gamma}, basal metabolism/min). Results: Stunning decreased SSA by 57% and Ees by 64%, without affecting MVO2, while increasing {alpha} by 71% and β by 134%, without affecting {gamma}. From the wasted oxygen, 72% was used for myofibrillar work and 18% for excitation–contraction coupling. EMD 60263 restored both {alpha} and β. Conclusions: Oxygen wastage in stunning is predominantly caused by a decreased myofibrillar efficiency and to a lesser extent by an increased oxygen cost of contractility. Considering that EMD 60263 reversed both causes of oxygen wastage, it is most likely that this drug increases myofibrillar Ca2+-sensitivity without increasing myofibrillar cross-bridge cycling.

KEYWORDS Stunning; e–c coupling; Oxygen consumption; Energy metabolism; Contractile apparatus


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