title: Heart function and molecular biological parameters are comparable in young adult and aged rats after chronic myocardial infarction.
abstract: OBJECTIVE
  To test the hypothesis that IL-1beta and IL-6 play a pivotal role after myocardial infarction (MI) particularly in aged rats.
  
  
  METHODS
  Chronic MI was induced in young adult (3.5 months) and aged (18 months) female Sprague-Dawley rats by ligation of the left coronary artery. Sham-operated animals of corresponding age served as controls. Heart function was measured by catheterization 4 weeks after MI. The expression of IL-1beta, IL-6, TGF-beta-isoforms, ANF, and components of the extracellular matrix (pro-collagen I and III, colligin, MMP-2 and TIMP2) was measured by ribonuclease protection assay.
  
  
  RESULTS
  Aged control rats differed from young adult rats in that LV-developed pressure (LVDP) was higher (161 vs. 147 mmHg, p<0.05) in response to the elevated total peripheral resistance (0.71 vs. 0.47 mmHg ml min/kg, p<0.05). Contractility was reduced in aged controls as indicated by decreased LV dP/dt (8.106 vs. 10.606 mmHg/s, p<0.05). LV function was severely depressed in both MI groups (reduction in LVDP by about 35% and LV dP/dt by about 30%, increase in LVEDP to 24 mmHg) while RVP and RV dP/dt markedly increased by about 100%. This was not different between both MI groups. ANF expression as a marker of hypertrophy was induced in both MI groups, but less pronounced in the LV of aged rats. Also, the mRNA expression pattern was qualitatively comparable, but showed gradual differences.
  
  
  CONCLUSIONS
  These results indicate that aged rats compensate well for hemodynamic overload induced by MI. Also, the mechanisms of myocardial post-MI remodeling are comparable in young adult and aged rats.
authors.affiliation: Carl-Ludwig-Institute of Physiology, Leipzig University, Liebigstr.27, D-04103 Leipzig, Germany. deta@medizin.uni-leipzig.de
authors.forename: Alexander
authors.initials: A
authors.lastname: Deten
authors.forename: Grit
authors.initials: G
authors.lastname: Marx
authors.forename: Wilfried
authors.initials: W
authors.lastname: Briest
authors.forename: Hans
authors.initials: H
authors.lastname: Christian Volz
authors.forename: Heinz-Gerd
authors.initials: HG
authors.lastname: Zimmer
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics; D015415:Biomarkers / Q000032:analysis; D024042:Collagen Type I / Q000235:genetics; D024061:Collagen Type III / Q000235:genetics; D016207:Cytokines / Q000235:genetics*; D005109:Extracellular Matrix / Q000276:immunology / Q000473:pathology; D005260:Female; D020778:Matrix Metalloproteinase 2 / Q000235:genetics; D023421:Models, Animal; D009203:Myocardial Infarction / Q000276:immunology* / Q000503:physiopathology; D009206:Myocardium / Q000276:immunology*; D020033:Protein Isoforms / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000235:genetics; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D024061:Collagen Type III; D016207:Cytokines; D020033:Protein Isoforms; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D019716:Tissue Inhibitor of Metalloproteinase-2; D009320:Atrial Natriuretic Factor; D020778:Matrix Metalloproteinase 2