Received July 10, 2006
Revised August 14, 2006
Accepted after revision October 9, 2006
Cardiovascular Control [210]
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Cardiovascular Hemodynamics and Ventriculo-Arterial Coupling in an Acute Pig Model of Ischemia-Reperfusion
Lieve Lanoye 1*,
Patrick Segers 2,
Vincent Tchana-Sato 3,
Stephanie Rolin 4,
Jean-Michel Dogne 4,
Alexandre Ghuysen 3,
Bernard Lambermont 3,
Julien Hanson 5,
Thomas Desaive 6,
Pascal Verdonck 2,
Vincent D'Orio 3,
Philippe Kolh 3
1 Ghent University, Belgium
2 Institute Biomedical Technology, Ghent University, Belgium
3 Hemodynamic Research Center (HemoLiège), University of Liège, Belgium
4 Department of Pharmacy, University of Namur, Belgium
5 Department of Medicinal Chemistry, University of Liège, Belgium
6 Thermodynamics of Irreversible Processes, University of Liège, Belgium
* To whom correspondence should be addressed. E-mail: lieve.lanoye{at}ugent.be.
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Abstract |
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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) hemodynamics and ventriculo-arterial (VA) coupling in acutely ischemic pigs. Experiments were performed in 6 animals, with measurements of cardiac and arterial function at baseline, after 60 minutes (T60) of ischemia and after 2 (T180) and 4 hours (T300) of reperfusion. Ventriculo-arterial coupling was assessed using the ventriculo-arterial elastance ratio (Ees/Ea) as well as using a "stiffness coupling" and "temporal coupling" index. Reperfusion following ischemia (T180 vs. T60) induced a progressive decline in cardiovascular function, evidenced by a decrease in mean arterial blood pressure, cardiac output and in 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. Ees/Ea 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 ischemic 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 Ees/Ea-ratio.
Key Words:
Contraction, Ischaemia, Perfusion
