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±0.2v4.9±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 assessedin vitroin 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.