title: Alterations of performance and oxygen utilization in chronically infarcted rat hearts.
abstract: Progressive dilatation of left ventricle has been demonstrated in hearts post-infarction. However, the relationship of performance and energy consumption in chronically infarcted heart has not been clarified. To address this problem, we measured left ventricular pressure and oxygen consumption (MVO2) during stepwise increases in left ventricular filling volume in isolated isovolumic buffer-perfused rat hearts 8 weeks after let coronary artery ligation or sham-operation. Systolic pressure-volume area (PVA) was calculated as an estimate of total mechanical energy consumed by the heart. The MVO2-PVA relation was analysed to define the economy of the contractile machinery in surviving myocardium. Structural dilatation and reduced pressure generation in infarcted hearts were indicated by a rightward shift of pressure-volume curves and a reduced maximal developed pressure of the left ventricle (80 +/- 5 v 119 +/- 4 mmHg, P < 0.01) which was obtained at substantially higher left ventricular volume compared to control hearts (0.79 +/- 0.02 v 0.39 +/- 0.01 ml, P < 0.01). The slope of the MVO2-PVA relation was significantly lower in the infarcted compared to the control groups (1.02 +/- 0.16 v 1.44 +/- 0.10 10(-5) mlO2/mmHg/ml, P < 0.05), reflecting an increased efficiency of chemomechanical energy transduction in surviving myocardium. However, at the similar MVO2 ventricular pressure development was significantly lower in infarcted hearts due to the unfavorable geometry resulting from ventricular dilatation.
authors.affiliation: Medizinische Universitätsklinik Würzburg, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Tian
authors.forename: P
authors.initials: P
authors.lastname: Gaudron
authors.forename: S
authors.initials: S
authors.lastname: Neubauer
authors.forename: K
authors.initials: K
authors.lastname: Hu
authors.forename: G
authors.initials: G
authors.lastname: Ertl
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000502:physiology; D002021:Buffers; D002908:Chronic Disease; D004734:Energy Metabolism / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D051381:Rats; D017208:Rats, Wistar
chemical_list: D002021:Buffers