Gosselin H, Qi X, Rouleau J L
Department of Medicine, Institut de cardiologie de Montréal, QC, Canada.
Can J Physiol Pharmacol. 1998 Jan;76(1):53-62.
Early after infarction, ventricular dysfunction occurs as a result of loss of myocardial tissue. Although papillary muscle studies suggest that reduced myocardial contractility contributes to this ventricular dysfunction, in vivo studies indicate that at rest, cardiac output is normal or near normal, suggesting that contractility of the remaining viable myocardium of the ventricular wall is preserved. However, this has never been verified. To explore this further, 100 rats with various-sized myocardial infarctions had ventricular function assessed by Langendorff preparation or by isolated papillary muscle studies 5 weeks after infarction. Morphologic studies were also done. Rats with large infarctions (54%) had marked ventricular dilatation (dilatation index from 0.23 to 0.75, p < 0.01) and papillary muscle dysfunction (total tension from 6.7 to 3.2 g/mm2, p < 0.01) but only moderate left ventricular dysfunction (maximum developed tension from 206 to 151 mmHg (1 mmHg = 133.3 Pa), p < 0.01), a decrease less than one would expect with an infarct size of 54%. The contractility of the remaining viable myocardium of the ventricle was also moderately depressed (peak systolic midwall stress 91 to 60 mmHg, p < 0.01). Rats with moderate infarctions (32%) had less marked but still moderate ventricular dilatation (dilatation index 0.37, p < 0.001) and moderate papillary muscle dysfunction (total tension 4.2 g/mm2, p < 0.01). However, their decrease in ventricular function was only mild (maximum developed pressure 178 mmHg, p < 0.01) and less than one would expect with an infarct size of 32%. The remaining viable myocardium of the ventricular wall appeared to have normal contractility (peak systolic midwall stress = 86 mmHg, ns). We conclude that in this postinfarction model, in large myocardial infarctions, a loss of contractility of the remaining viable myocardium of the ventricular wall occurs as early as 5 weeks after infarction and that papillary muscle studies slightly overestimate the degree of ventricular dysfunction. In moderate infarctions, the remaining viable myocardium of the ventricular wall has preserved contractility while papillary muscle function is depressed. In this relatively early postinfarction phase, ventricular remodelling appears to help maintain left ventricular function in both moderate and large infarctions.
梗死早期，由于心肌组织丧失，心室功能出现障碍。尽管乳头肌研究表明心肌收缩力降低是导致这种心室功能障碍的原因之一，但体内研究表明，在静息状态下，心输出量正常或接近正常，这表明心室壁剩余存活心肌的收缩力得以保留。然而，这一点从未得到证实。为了进一步探究这一问题，对100只患有不同大小心肌梗死的大鼠在梗死后5周通过Langendorff灌流法或分离乳头肌研究来评估心室功能。同时也进行了形态学研究。梗死面积较大的大鼠（54%）出现明显的心室扩张（扩张指数从0.23至0.75，p<0.01）和乳头肌功能障碍（总张力从6.7至3.2 g/mm2，p<0.01），但仅有中度左心室功能障碍（最大舒张期压力从206至151 mmHg（1 mmHg = 133.3 Pa），p<0.01），其降低程度小于梗死面积为54%时预期的降低程度。心室壁剩余存活心肌的收缩力也有中度降低（收缩期峰值中壁应力从91至60 mmHg，p<0.01）。梗死面积中等的大鼠（32%）心室扩张程度较轻但仍为中度（扩张指数0.37，p<0.001），乳头肌功能障碍为中度（总张力4.2 g/mm2，p<0.01）。然而，它们的心室功能降低仅为轻度（最大舒张期压力178 mmHg，p<0.01），且小于梗死面积为32%时预期的降低程度。心室壁剩余存活心肌似乎具有正常的收缩力（收缩期峰值中壁应力 = 86 mmHg，无显著性差异）。我们得出结论，在这个心肌梗死后模型中，在大面积心肌梗死时，心室壁剩余存活心肌的收缩力在梗死后5周就开始丧失，并且乳头肌研究略微高估了心室功能障碍的程度。在中等面积梗死时，心室壁剩余存活心肌的收缩力得以保留，而乳头肌功能降低。在这个相对较早的心肌梗死后阶段，心室重构似乎有助于在中等面积梗死和大面积梗死时维持左心室功能。
