Hanatani A, Yoshiyama M, Kim S, Omura T, Ikuno Y, Takeuchi K, Iwao H, Yoshikawa J
First Department of Internal Medicine, Osaka City University Medical School, Japan.
Jpn Heart J. 1998 May;39(3):375-88. doi: 10.1536/ihj.39.375.
The purpose of this study was to examine left ventricular function and cardiac gene expressions at an acute phase after myocardial infarction (MI). MI was induced in rats by ligation of the left coronary artery. Two days after MI, we performed Doppler-echocardiography and measured the systolic and diastolic function. We then analyzed the contractile protein and extracellular matrix mRNAs of cardiac tissues in the infarcted region, including the adjacent noninfarcted myocardium (the adjacent noninfarcted myocardium) and the remote noninfarcted myocardium, by Northern blot hybridization. Fractional shortening decreased significantly to 28%. Peak early diastolic filling wave (E wave) velocity increased in MI rats (MI; 90 +/- 3 cm/s versus the control; 71 +/- 2 cm/s, p < 0.05), and the deceleration rate of the E wave velocity was more rapid in MI rats (MI; 22.0 +/- 2.6 m/s2 versus the control; 16.5 +/- 2.0 m/s2, p < 0.01). Atrial filling wave (A wave) velocity decreased, resulting in a marked increase in the ratio of E wave to A wave velocity (MI; 3.1 +/- 0.3 versus the control; 2.1 +/- 0.2, p < 0.01). In the adjacent noninfarcted myocardium, mRNA levels for alpha-skeletal actin, atrial natriuretic polypeptide (ANP), transforming growth factor-beta 1(TGF-beta 1), fibronectin, and collagen types I and III increased significantly. In the remote noninfarcted myocardium, mRNA levels for alpha-skeletal actin, ANP, and collagen types I and III increased, while mRNA levels for beta-myosin heavy chain, TGF-beta 1 and fibronectin did not change. We observed left ventricular dysfunction and different gene expression between adjacent noninfarcted myocardium and in the remote noninfarcted myocardium two days after MI. These findings suggest that cardiac gene expression after MI may be a compensation reaction for cardiac dysfunction induced by myocardial damage.
本研究的目的是检测心肌梗死（MI）急性期的左心室功能和心脏基因表达。通过结扎左冠状动脉在大鼠中诱导MI。MI后两天，我们进行了多普勒超声心动图检查并测量了收缩和舒张功能。然后，我们通过Northern印迹杂交分析了梗死区域心脏组织的收缩蛋白和细胞外基质mRNA，包括相邻的非梗死心肌（相邻的非梗死心肌）和远处的非梗死心肌。缩短分数显著降低至28%。MI大鼠的舒张早期充盈波（E波）峰值速度增加（MI；90±3cm/s，对照组；71±2cm/s，p<0.05），且MI大鼠的E波速度减速更快（MI；22.0±2.6m/s²，对照组；16.5±2.0m/s²，p<0.01）。心房充盈波（A波）速度降低，导致E波与A波速度比值显著增加（MI；3.1±0.3，对照组；2.1±0.2，p<0.01）。在相邻的非梗死心肌中，α-骨骼肌动蛋白、心钠素（ANP）、转化生长因子-β1（TGF-β1）、纤连蛋白以及I型和III型胶原蛋白的mRNA水平显著增加。在远处的非梗死心肌中，α-骨骼肌动蛋白、ANP以及I型和III型胶原蛋白的mRNA水平增加，而β-肌球蛋白重链、TGF-β1和纤连蛋白的mRNA水平没有变化。我们观察到MI后两天相邻的非梗死心肌和远处的非梗死心肌之间存在左心室功能障碍和不同的基因表达。这些发现表明，MI后的心脏基因表达可能是对心肌损伤诱导的心脏功能障碍的一种代偿反应。
