Constitutive properties of adult mammalian cardiac muscle cells

Article

关键词: LEFT-VENTRICULAR HYPERTROPHY;    AORTIC-VALVE DISEASE;    DIASTOLIC DYSFUNCTION;    CONTRACTILE DYSFUNCTION;    VISCOELASTIC PROPERTIES;    MYOCARDIAL STRUCTURE;    CYTOSKELETAL ROLE;    ACTIVE TENSION;    HEART-FAILURE;    MYOCYTES;   

DOI  :  10.1161/01.CIR.98.6.567

来源: SCIE

【 摘 要 】

Background-The purpose of this study was to determine whether changes in the constitutive properties of the cardiac muscle cell play a causative role in the development of diastolic dysfunction. Methods and Results-Cardiocytes from normal and pressure-hypertrophied cats were embedded in an agarose gel, placed on a stretching device, and subjected to a change in stress (sigma), and resultant changes in cell strain (epsilon) were measured. These measurements were used to examine the passive elastic spring, viscous damping, and myofilament activation. The passive elastic spring was assessed in protocol A by increasing the sigma on the agarose gel at a constant rate to define the cardiocyte sigma-versus-epsilon relationship. Viscous damping was assessed in protocol B from the loop area between the cardiocyte sigma-versus-epsilon relationship during an increase and then a decrease in sigma. In both protocols, myofilament activation was minimized by a reduction in [Ca2+](i). Myofilament activation effects were assessed in protocol C by defining cardiocyte sigma versus epsilon during an increase in sigma with physiological [Ca2+](i). In protocol A, the cardiocyte sigma-versus-epsilon relationship was similar in normal and hypertrophied cells. In protocol B, the loop area was greater in hypertrophied than normal cardiocytes. In protocol C, the sigma-versus-epsilon relation in hypertrophied cardiocytes was shifted to the left compared with normal cells. Conclusions-Changes in viscous damping and myofilament activation in combination may cause pressure-hypertrophied cardiocytes to resist changes in shape during diastole and contribute to diastolic dysfunction.

【 授权许可】

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