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. (C) 1998 Academic Press.