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This Article Full Text Full Text (PDF) All Versions of this Article: 92/1/127    most recent expphysiol.2006.034983v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lanoye, L. Articles by Kolh, P. Search for Related Content PubMed PubMed Citation Articles by Lanoye, L. Articles by Kolh, P.

¹ Cardiovascular Mechanics and Biofluid Dynamics, Institute Biomedical Technology, Ghent University, Belgium ² Haemodynamic Research Center (HemoLiège)³ Department of Pharmacy, University of Namur, Belgium⁴ Department of Medicinal Chemistry⁵ Thermodynamics of Irreversible Processes, University of Liège, Belgium

Although reperfusion after coronary occlusion is mandatory for myocardial salvage, reperfusion may trigger a cascade of harmful events (reperfusion injury) adding to myocardial injury. We investigated effects of reperfusion on left ventricular (LV) haemodynamics and ventriculo-arterial (VA) coupling in pigs following acute myocardial ischaemia induced by coronary artery occlusion. Experiments were performed in six animals, with measurements of cardiac and arterial function at baseline, after 60 min of ischaemia (T60) and after 2 (T180) and 4 h of reperfusion (T300). Ventriculo-arterial coupling was assessed using the ventriculo-arterial elastance ratio of paper, as well as using a ‘stiffness coupling’ and ‘temporal coupling’ index. Reperfusion following ischaemia (T180 versus T60) induced a progressive decline in cardiovascular function, evidenced by a decrease in mean arterial blood pressure, cardiac output and ejection fraction which was not restored at T300. Although reperfusion also induced an increase in slope of the end-systolic pressure–volume relationship (ESPVR), the ESPVR curve shifted to the right, associated with a depression of contractile function. Histology demonstrated irreversible myocardial damage at T300. The ventriculo-arterial elastance ratio and the ‘stiffness coupling’ index were unaffected throughout the protocol, but the ‘temporal coupling’ parameter indicated a relative shift between heart period and the time constant of the arterial system. It is unlikely that these alterations are attributable to ischaemic injury alone. The combination of both the stiffness and temporal coupling index may provide more information when studying ventriculo-arterial coupling than the more commonly used ventricular end-systolic stiffness/effection arterial elastance (E_es/E_a) ratio.

(Received 10 July 2006; accepted after revision 9 October 2006; first published online 12 October 2006)
Corresponding author L. Lanoye: Hydraulics Laboratory, Institute Biomedical Technology, St-Pietersnieuwstraat 41, 9000 Gent, Belgium. Email: lieve.lanoye{at}ugent.be