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扩张型心肌病清醒犬心肌收缩力的改变

Alterations in myocardial contractility in conscious dogs with dilated cardiomyopathy.

作者信息

Shannon R P, Komamura K, Stambler B S, Bigaud M, Manders W T, Vatner S F

机构信息

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

Am J Physiol. 1991 Jun;260(6 Pt 2):H1903-11. doi: 10.1152/ajpheart.1991.260.6.H1903.

Abstract

We investigated the changes in left ventricular (LV) geometry and myocardial contractility in eight conscious chronically instrumented dogs studied before and after the development of dilated cardiomyopathy induced by rapid ventricular pacing. Significant increases (P less than 0.01) were observed in cardiac dimensions in both the LV long and short axes and in end-diastolic volume (control: 53 +/- 1 ml; cardiomyopathy: 76 +/- 2 ml) and end-systolic volume (control: 27 +/- 2 ml; cardiomyopathy: 56 +/- 7 ml). This was associated with the left ventricle assuming a more spherical shape with LV long-to-short axis ratio falling from 1.59 +/- 0.05 to 1.47 +/- 0.04 (P less than 0.05). Both isovolumic (LV dP/dt) and ejection phase indexes (LV mean velocity of circumferential fiber shortening, corrected LV short-axis diameter at point of maximum shortening, and LV ejection fraction) were depressed by 50%. The end-systolic elastance was also depressed significantly (control: 16.6 +/- 0.7 g.cm-2.ml-1; cardiomyopathy: 10.1 +/- 1.7 g.cm-2.ml-1, P less than 0.02). However, cardiac output was maintained at 3 wk due to a compensatory tachycardia (+31 +/- 3 beats/min), plasma volume expansion (+295 +/- 68 ml, P less than 0.05), and greater reliance on the Frank-Starling mechanism. However, in an additional four dogs studied at 4-5 wk, cardiac output fell significantly (P less than 0.05). Thus rapid ventricular pacing results in dilated congestive cardiomyopathy in conscious dogs characterized by globally depressed myocardial systolic function and changes in LV shape.

摘要

我们研究了八只清醒的慢性植入仪器的犬在快速心室起搏诱发扩张型心肌病前后左心室(LV)几何形状和心肌收缩性的变化。观察到左心室长轴和短轴的心脏尺寸、舒张末期容积(对照:53±1ml;心肌病:76±2ml)和收缩末期容积(对照:27±2ml;心肌病:56±7ml)均显著增加(P<0.01)。这与左心室呈更球形的形状相关,左心室长轴与短轴之比从1.59±0.05降至1.47±0.04(P<0.05)。等容(左心室dP/dt)和射血期指标(左心室圆周纤维缩短平均速度、最大缩短点处校正后的左心室短轴直径和左心室射血分数)均降低了50%。收缩末期弹性也显著降低(对照:16.6±0.7g.cm-2.ml-1;心肌病:10.1±1.7g.cm-2.ml-1,P<0.02)。然而,由于代偿性心动过速(+31±3次/分钟)、血浆容量扩张(+295±68ml,P<0.05)以及对Frank-Starling机制的更大依赖,心输出量在3周时维持不变。然而,在另外四只4-5周时研究的犬中,心输出量显著下降(P<0.05)。因此,快速心室起搏导致清醒犬发生扩张型充血性心肌病,其特征为整体心肌收缩功能降低和左心室形状改变。

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