© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Ischemic preconditioning reduces unloaded myocardial oxygen consumption in an in-vivo sheep model*
aCenter for Experimental Surgery and Anaesthesiology (C.E.H.A.), Cardiovascular Research Unit, Katholieke Universiteit Leuven, Minderbroedersstraat 17, Leuven, Belgium
bDepartment of Pathology, Katholieke Universiteit Leuven, Leuven, Belgium
willem.flameng{at}med.kuleuven.ac.be
* Presented in part at the XXIII Congress of European Society of Cardiology, Stockholm, 1–5 September 2001.
* Corresponding author. Tel.: +32-16-337-298; fax: +32-16-337-855
Objective: Ischemic preconditioning (IP) describes the adaptation of the myocardium to ischemic stress preceded by short periods of ischemia and reperfusion. However, its cardioprotective mechanisms are not completely understood. We assessed the effect of IP on ventricular energetics in an in-vivo sheep model. Methods: IP was performed in six sheep by three 5 min aortic cross-clamping periods interspersed with 5 min of reperfusion during cardiopulmonary bypass and with six sheep as time-matched controls. Global myocardial ischemia was subsequently achieved by 30 min aortic cross-clamping with left ventricular unloading during normothermic cardiopulmonary bypass. Weaning from cardiopulmonary bypass was performed 40 min after reperfusion. At baseline, after treatment (IP or time-matched cardiopulmonary bypass), and up to 100 min after reperfusion, left ventricular pressure–volume loops were measured using a conductance catheter during a right heart bypass preparation. Contractility, diastolic function, and ventriculo–arterial coupling were evaluated. Ventricular energetics [the relation between myocardial oxygen consumption (MVO2) and systolic pressure–volume area (PVA)] was also evaluated. A right heart bypass was instituted to control the preload and to decompress the right ventricle completely, thereby eliminating parallel conductance variation and minimizing the contribution of the right ventricle to MVO2. Results: IP reduced unloaded MVO2 (PVA-independent MVO2). Contractility, diastolic function, and ventriculo–arterial coupling in the IP group were better preserved than in the control group after ischemia-reperfusion. Conclusions: IP reduces unloaded MVO2, and preserves contractility, diastolic function, and ventriculo–arterial coupling after 30 min global myocardial ischemia in an in-vivo sheep model.
KEYWORDS Ischemia; Oxygen consumption; Preconditioning; Reperfusion; Ventricular function
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