Eberli F R, Sam F, Ngoy S, Apstein C S, Colucci W S
Cardiac Muscle Research Laboratory, Boston University School of Medicine, MA 92118, USA.
J Mol Cell Cardiol. 1998 Jul;30(7):1443-7. doi: 10.1006/jmcc.1998.0702.
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.
本研究的目的是确定等容收缩的Langendorff心脏是否可用于评估心肌梗死后小鼠心脏左心室容积和收缩储备的变化。通过结扎左前降支冠状动脉，在CD-1小鼠中诱导心肌梗死（梗死面积占左心室重量的40±3%）。梗死后两周，非梗死心室出现代偿性肥大，表现为心脏与体重比增加（5.5±0.2对4.9±0.2mg/g；P<0.05；n=12）以及心房利钠肽mRNA表达增加（4.4±1.4倍；P<0.001；n=4）。在体外，用补充红细胞的缓冲液（血细胞比容=40%）灌注等容收缩的心脏，评估左心室压力-容积关系。心肌梗死导致左心室扩张，舒张期压力-容积关系向右移位。这与左心室收缩功能降低有关，在一系列左心室容积范围内，舒张末期压力降低即证明了这一点。因此，使用等容收缩的Langendorff标本评估小鼠心肌梗死后左心室重构的结构和功能后果是可行的。
