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大鼠去表皮心肌细胞力学特性的肌节长度依赖性:对肌球蛋白重链的依赖性

Sarcomere length dependence of rat skinned cardiac myocyte mechanical properties: dependence on myosin heavy chain.

作者信息

Korte F Steven, McDonald Kerry S

机构信息

Department of Physiology, School of Medicine, University of Missouri, Columbia, MO, USA.

出版信息

J Physiol. 2007 Jun 1;581(Pt 2):725-39. doi: 10.1113/jphysiol.2007.128199. Epub 2007 Mar 8.

Abstract

The effects of sarcomere length (SL) on sarcomeric loaded shortening velocity, power output and rates of force development were examined in rat skinned cardiac myocytes that contained either alpha-myosin heavy chain (alpha-MyHC) or beta-MyHC at 12 +/- 1 degrees C. When SL was decreased from 2.3 microm to 2.0 microm submaximal isometric force decreased approximately 40% in both alpha-MyHC and beta-MyHC myocytes while peak absolute power output decreased 55% in alpha-MyHC myocytes and 70% in beta-MyHC myocytes. After normalization for the fall in force, peak power output decreased about twice as much in beta-MyHC as in alpha-MyHC myocytes (41% versus 20%). To determine whether the fall in normalized power was due to the lower force levels, [Ca(2+)] was increased at short SL to match force at long SL. Surprisingly, this led to a 32% greater peak normalized power output at short SL compared to long SL in alpha-MyHC myocytes, whereas in beta-MyHC myocytes peak normalized power output remained depressed at short SL. The role that interfilament spacing plays in determining SL dependence of power was tested by myocyte compression at short SL. Addition of 2% dextran at short SL decreased myocyte width and increased force to levels obtained at long SL, and increased peak normalized power output to values greater than at long SL in both alpha-MyHC and beta-MyHC myocytes. The rate constant of force development (k(tr)) was also measured and was not different between long and short SL at the same [Ca(2+)] in alpha-MyHC myocytes but was greater at short SL in beta-MyHC myocytes. At short SL with matched force by either dextran or [Ca(2+)], k(tr) was greater than at long SL in both alpha-MyHC and beta-MyHC myocytes. Overall, these results are consistent with the idea that an intrinsic length component increases loaded crossbridge cycling rates at short SL and beta-MyHC myocytes exhibit a greater sarcomere length dependence of power output.

摘要

在12±1℃下,对含有α-肌球蛋白重链(α-MyHC)或β-肌球蛋白重链(β-MyHC)的大鼠去表皮心肌细胞,研究了肌节长度(SL)对肌节加载缩短速度、功率输出和力发展速率的影响。当SL从2.3微米降至2.0微米时,亚最大等长力在α-MyHC和β-MyHC心肌细胞中均下降约40%,而α-MyHC心肌细胞的峰值绝对功率输出下降55%,β-MyHC心肌细胞下降70%。在力下降进行归一化后,β-MyHC心肌细胞的峰值功率输出下降幅度约为α-MyHC心肌细胞的两倍(41%对20%)。为确定归一化功率下降是否由于较低的力水平,在短SL时增加[Ca(2+)]以使力与长SL时匹配。令人惊讶的是,这导致α-MyHC心肌细胞在短SL时的峰值归一化功率输出比长SL时高32%,而在β-MyHC心肌细胞中,短SL时峰值归一化功率输出仍较低。通过在短SL时对心肌细胞进行压缩,测试了细丝间距在确定功率的SL依赖性中所起的作用。在短SL时添加2%葡聚糖可减小心肌细胞宽度并将力增加至长SL时的水平,且在α-MyHC和β-MyHC心肌细胞中均将峰值归一化功率输出增加至高于长SL时的值。还测量了力发展的速率常数(k(tr)),在相同[Ca(2+)]下,α-MyHC心肌细胞中长SL和短SL时的k(tr)无差异,但β-MyHC心肌细胞中短SL时的k(tr)更大。在短SL时,通过葡聚糖或[Ca(2+)]使力匹配,α-MyHC和β-MyHC心肌细胞中的k(tr)均大于长SL时。总体而言,这些结果与以下观点一致,即内在长度成分在短SL时增加加载的横桥循环速率,且β-MyHC心肌细胞的功率输出表现出更大的肌节长度依赖性。

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