Left-ventricular structural and functional remodeling in the mouse after myocardial infarction: assessment with the isovolumetrically-contracting Langendorff heart.
The goal of this study was to determine whether the isovolumically-contracting Langendorff heart could be used to assess changes in left-ventricular volume and contractile reserve in the mouse heart after myocardial infarction. Myocardial infarction (40 +/- 3% of the left ventricle by weight) was induced in CD-1 mice by ligation of the left-anterior descending coronary artery. Two weeks after infarction there was compensatory hypertrophy of the non-infarcted ventricle as indicated by increases in heart-to-body weight ratio (5.5 +/- 0.2 v 4.9 +/- 0.2 mg/g; P < 0.05; n = 12) and the expression of atrial natriuretic peptide mRNA (4.4 +/- 1.4-fold; P < 0.001; n = 4). Left-ventricular pressure-volume relationships were assessed in vitro in isovolumically-contracting hearts perfused with red cell-supplemented buffer (hematrocrit = 40%). Myocardial infarction caused left-ventricular dilation with a rightward-shift of the diastolic pressure-volume relationship. This was associated with reduced left-ventricular contractile function, as evidenced by a decrease in developed pressure over a range of left-ventricular volumes. Thus, it is feasible to use the isovolumically-contracting Langendorff preparation to assess the structural and functional consequences of left-ventricular remodeling in the mouse after a myocardial infarction.
Eberli
F R
FR
Cardiac Muscle Research Laboratory, Boston University School of Medicine, MA 92118, USA.
Sam
F
F
Ngoy
S
S
Apstein
C S
CS
Colucci
W S
WS
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics; D004195:Disease Models, Animal; D066298:In Vitro Techniques; D051379:Mice; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology*; D010477:Perfusion; D012333:RNA, Messenger; D020257:Ventricular Remodeling / Q000502:physiology*
D012333:RNA, Messenger; D009320:Atrial Natriuretic Factor