Bioenergetic, functional and morphological consequences of postinfarct cardiac remodeling in the rat.
Despite recent advances in the treatment, severe chronic heart failure (CHF) remains a syndrome associated with high mortality. Therefore, the search for new agents to improve both patient symptoms and survival, as well as the pursuit for detailed knowledge about pathophysiology of the failing heart, will continue to depend on relevant animal models. Large acute myocardial infarction (MI) initiates complex changes in the geometrical, structural, and biochemical architecture of both infarcted and non-infarcted regions of ventricular myocardium, which can profoundly affect left ventricular function and prognosis. In this paper we present a new model for non-invasive cardiac (31)P MRS in the rat. Volume-selective (31)P magnetic resonance spectroscopy and echocardiography were used for evaluation of myocardial energy metabolism, cardiac morphology and function in rats 3 days and 3 weeks after induction of large MI. The phosphocreatine:adenosine triphosphate (PCr:ATP) ratio was decreased in rats with MI comparing with controls both at 3 days (1.6+/-0.06 vs 2.7+/-0.04; mean+/-s.e.m. P<0.0001) and 3 weeks (1.6+/-0.07 v 2.7+/-0.02 P<0.0001) postinfarct. The results from the study demonstrate that postinfarct cardiac remodeling is a rapid process of changes not only in cardiac geometry, structure and function but also in myocardial energy metabolism after large transmural MI in the rat.
Omerovic
E
E
Wallenberg Laboratories, Sahlgrenska University Hospital, Göteborg, Sweden.
Bollano
E
E
Basetti
M
M
Kujacic
V
V
Waagstein
L
L
Hjalmarson
A
A
Waagstein
F
F
Soussi
B
B
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003971:Diastole; D004195:Disease Models, Animal; D004452:Echocardiography; D004734:Energy Metabolism; D006339:Heart Rate; D006352:Heart Ventricles; D006439:Hemodynamics / Q000502:physiology*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013599:Systole; D016277:Ventricular Function, Left / Q000502:physiology
D010725:Phosphocreatine; D000255:Adenosine Triphosphate