title: Regional biochemical remodeling in non-infarcted tissue of rat heart post-myocardial infarction.
abstract: Changes in the capacities of ATP-synthesizing reactions were analysed in residual non-infarcted myocardium following myocardial infarction. Rats were subjected to left coronary artery ligation (MI; n = 11) or to sham operation (sham; n = 18). Two months later, hearts were excised, rinsed and buffer-perfused isovolumically. In vitro pressure-volume relationships were recorded. After separation into left and right ventricles (LV, RV) and atria (LA, RA), samples were analysed for citrate synthase, glycolytic enzymes (phosphofructokinase, glyceraldehyde-3-phosphate-dehydrogenase, lactate dehydrogenase (LDH) and its isoforms) and the creatine kinase (CK) system [total CK, CK isoenzymes (CKBB, CKMB, CKMM and CKmito) and total creatine]. In residual intact heart, citrate synthase activity and activities of most glycolytic enzymes were unchanged, but LDH activity and anaerobic LDH isoenzymes increased significantly. Total creatine kinae activity (6.5 +/- 0.2 IU/mg protein in sham LV) was decreased by chronic myocardial infarction in LV (5.4 +/- 0.3, with P < 0.05 sham v MI) but not in RV (6.2 +/- 0.2). Significant CK isoenzyme shifts occurred in both ventricles "adult" CKmito (32.5 +/- 1.4% in sham LV) was reduced in LV (22.1 +/- 2.1% with P < 0.05 sham v MI) and in RV (19.2 +/- 2.9%, with P < 0.05 sham v MI), "fetal" CKBB and CKMB increased. Total creatine content was reduced by up to 35% in both ventricles. In sham hearts atria had lower total and mitochondrial CK activity, lower total creatine content and higher CKMB and CKBB activity compared to ventricles; however, myocardial infarction induced changes directionally comparable to the changes observed in ventricles. Thus, 2 months after myocardial infarction changes of the capacities of ATP synthesizing reactions are comparable for all heart chambers, with the exception of total CK activity decreasing only in left ventricular tissue.
authors.affiliation: II. Medizinischen Klinik, Mannheim/Heidelberg University, FRG.
authors.forename: A
authors.initials: A
authors.lastname: Laser
authors.forename: J S
authors.initials: JS
authors.lastname: Ingwall
authors.forename: R
authors.initials: R
authors.lastname: Tian
authors.forename: I
authors.initials: I
authors.lastname: Reis
authors.forename: K
authors.initials: K
authors.lastname: Hu
authors.forename: P
authors.initials: P
authors.lastname: Gaudron
authors.forename: G
authors.initials: G
authors.lastname: Ertl
authors.forename: S
authors.initials: S
authors.lastname: Neubauer
mesh_terms: D000818:Animals; D002950:Citrate (si)-Synthase / Q000378:metabolism*; D003402:Creatine Kinase / Q000378:metabolism*; D006321:Heart / Q000503:physiopathology; D007527:Isoenzymes / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism*; D009203:Myocardial Infarction / Q000201:enzymology* / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology*; D010732:Phosphofructokinase-1 / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D017725:Ventricular Pressure
chemical_list: D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase; D002950:Citrate (si)-Synthase; D010732:Phosphofructokinase-1; D003402:Creatine Kinase