title: Myocardial contractile efficiency increases in proportion to a fetal enzyme shift in chronically infarcted rat hearts.
abstract: Changes in creatine kinase (CK) and lactate dehydrogenase (LDH) isoform expression occur in residual tissue after myocardial infarction. It is unknown how these changes correlate with cardiac remodeling, contractile performance and efficiency. Rats were subjected to left coronary artery ligation (MI) or sham operation (sham). Left ventricular end-diastolic pressure (EDP) was measured in vivo 8 weeks later. Hearts were isolated, buffer-perfused (Langendorff) at constant pressure and isovolumetric left ventricular (LV) pressure-volume (PV) curves were recorded. LV PV areas (PVA) were calculated and related to oxygen consumption. Biopsies of intact left ventricular tissue were taken for biochemical measurements. Correlations between in vivo EDP and biochemical parameters were found: Total CK activity (r = -.47, p = .022), CK isoenzyme percentage for BB (r = +.57, p = .004), MB (r = +.54, p = .006) and CK-mito (r = -.51, p = .012), total creatine content (r = -.61, p = .002) and the ratio of LDH5/LDH1 (r = .49, p = .016). Correlations were also detected for left ventricular volume and PVAs at in vivo EDP demonstrating that the extent of CK and LDH system alterations correlate with the extent of LV dilatation and mechanical energy requirements. The slope of the MVO(2)-PVA relation decreased significantly with increasing values of in vivo EDP (r = -.68, p = 0.0003) indicating increased contractile ef.ciency. Improved efficiency correlated with the increase in fetal CK isoenzyme expression. Thus, contractile efficiency increases parallel to the extent of left ventricular dilatation and dysfunction. CK and LDH system changes in residual intact myocardium also occur proportional to LV dysfunction.
authors.affiliation: Medizinische Universitätsklinik Würzburg, Würzburg, Germany.
authors.forename: Anne
authors.initials: A
authors.lastname: Naumann
authors.forename: Stefan
authors.initials: S
authors.lastname: Neubauer
authors.forename: Peter
authors.initials: P
authors.lastname: Kuhlencordt
authors.forename: Kai
authors.initials: K
authors.lastname: Hu
authors.forename: Rong
authors.initials: R
authors.lastname: Tian
authors.forename: Peter
authors.initials: P
authors.lastname: Gaudron
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
mesh_terms: D000818:Animals; D002908:Chronic Disease; D003402:Creatine Kinase / Q000378:metabolism*; D004195:Disease Models, Animal; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000378:metabolism*; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000150:complications / Q000201:enzymology* / Q000503:physiopathology*; D009206:Myocardium / Q000201:enzymology*; D010101:Oxygen Consumption; D051381:Rats; D017208:Rats, Wistar; D018487:Ventricular Dysfunction, Left / Q000201:enzymology / Q000209:etiology* / Q000503:physiopathology; D017725:Ventricular Pressure
chemical_list: D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase