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首页> 外文期刊>American Journal of Physiology >Constitutive properties of hypertrophied myocardium: cellular contribution to changes in myocardial stiffness.
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Constitutive properties of hypertrophied myocardium: cellular contribution to changes in myocardial stiffness.

机译：肥厚型心肌的组成特性：细胞对心肌硬度变化的贡献。

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摘要

Recent studies have suggested that pressure overload hypertrophy (POH) alters the viscoelastic properties of individual cardiocytes when studied in isolation. However, whether these changes in cardiocyte properties contribute causally to changes in the material properties of the cardiac muscle as a whole is unknown. Accordingly, a selective, isolated, acute change in cardiocyte constitutive properties was imposed in an in vitro system capable of measuring the resultant effect on the material properties of the composite cardiac muscle. POH caused an increase in both myocardial elastic stiffness, from 20.5 +/- 1.3 to 28.4 +/- 1.8, and viscous damping, from 15.2 +/- 1.1 to 19.8 +/- 1.5 s (normal vs. POH, P < 0.05), respectively. Recent studies have shown that cardiocyte constitutive properties could be acutely altered by depolymerizing the microtubules with colchicine. Colchicine caused a significant decrease in the viscous damping in POH muscles (19.8 +/- 1.5 s at baseline vs. 14.7 +/- 1.3 s after colchicine, P < 0.05). Therefore, myocardial material properties can be altered by selectively changing the constitutive properties of one element within this muscle tissue, the cardiocyte. Changes in the constitutive properties of the cardiocytes themselves contribute to the abnormalities in myocardial stiffness and viscosity that develop during POH.
机译：最近的研究表明，单独进行研究时，压力超负荷肥大（POH）会改变单个心肌细胞的粘弹性质。然而，尚不清楚这些心肌细胞特性的变化是否整体上导致了心肌材料特性的变化。因此，在体外系统中，选择性地，孤立地，急性地改变了心肌的组成特性，该体外系统能够测量对复合心肌材料特性的最终影响。 POH引起的心肌弹性刚度从20.5 +/- 1.3增至28.4 +/- 1.8，粘性阻尼从15.2 +/- 1.1增至19.8 +/- 1.5 s（正常值与POH相比，P <0.05） ， 分别。最近的研究表明，通过用秋水仙碱解聚微管，可以急性改变心肌细胞的组成特性。秋水仙碱导致POH肌肉的粘滞阻尼显着降低（基线时为19.8 +/- 1.5 s，而秋水仙碱后为14.7 +/- 1.3 s，P <0.05）。因此，可以通过选择性地改变该肌肉组织内的一种元素即心肌细胞的构成特性来改变心肌材料的特性。心肌细胞本身的组成特性的变化会导致POH期间出现的心肌僵硬和粘度异常。

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