ter Keurs H E, de Tombe P P
University of Calgary, Health Sciences Centre, Alberta, Canada.
Adv Exp Med Biol. 1993;332:649-64; discussion 664-5. doi: 10.1007/978-1-4615-2872-2_58.
Maximal unloaded velocity of shortening of cardiac muscle (Vo) depends on the level of activation of the contractile filaments. We have tested the hypothesis that this dependence may be caused by viscous resistance of the muscle to length changes. Twitch force (Fo) and sarcomere shortening were studied in trabeculae dissected from the right ventricle of rat myocardium, superfused with modified Krebs-Henseleit solution at 25 degrees C. Sarcomere length (SL) was measured by laser diffraction techniques; force was measured by a silicon strain gauge; velocity of sarcomere shortening was measured using the "isovelocity release" technique. Vo and Fo at slack SL were a sigmoidal function of [Ca2+]o, but Vo was more sensitive to [Ca2+]o (Km: 0.44 +/- 0.04 mM) than isometric twitch force (Km: 0.68 +/- 0.03 mM). At [Ca2+]o = 1.5 mM, Vo was independent of SL above 1.9 microns, but depended on SL at lower [Ca2+]o and always depended on SL < 1.9 microns. A constant relation was observed between Vo and Fo, irrespective whether Fo was altered by variation of [Ca2+]o or SL above slack length. Visco-elastic properties of unstimulated muscles were studied at SL = 2.0 microns by small linear length changes at varied velocities up to 40 microns/s. The force response to stretch, after correction for the contribution of static parallel elasticity, consisted of an exponential increase of force (tau = 4 ms) and an exponential decline after the stretch. This response would be expected from an arrangement of a viscous element in series with an elastic element. Viscous force increased in proportion to stretch velocity by 0.2-0.5% of Fo/micron/s up to 15 microns/s, while the calculated stiffness of the elastic component was 25-45 N.mm-3, suggesting that the most likely structural candidate for this visco-elastic element is titin. Dynamic stiffness at 500 Hz was proportional to instantaneous force during shortening and was 12% of stiffness at maximal twitch force when shortening occurred at Vo. This suggests that the number of active force generators, even at maximal activation, is strongly reduced during shortening at Vo. The observed relation between Vo and Fo could be explained by a model in which shortening velocity of the cardiac sarcomere depends on the level of activation and hence on the number of cross bridges supporting the viscous load.
心肌最大无负荷缩短速度（Vo）取决于收缩细丝的激活水平。我们检验了这样一种假说，即这种依赖性可能是由肌肉对长度变化的粘性阻力引起的。在从大鼠心肌右心室分离出的小梁中研究了单收缩力（Fo）和肌节缩短情况，小梁在25℃下用改良的克雷布斯 - 亨塞尔特溶液进行灌流。通过激光衍射技术测量肌节长度（SL）；用硅应变片测量力；使用“等速释放”技术测量肌节缩短速度。松弛SL时的Vo和Fo是[Ca2+]o的S形函数，但Vo比等长单收缩力对[Ca2+]o更敏感（Km：0.44±0.04 mM）（等长单收缩力的Km：0.68±0.03 mM）。在[Ca2+]o = 1.5 mM时，SL大于1.9微米时Vo与SL无关，但在较低[Ca2+]o时Vo取决于SL，且SL < 1.9微米时Vo总是取决于SL。无论Fo是通过改变[Ca2+]o还是通过改变松弛长度以上的SL来改变，Vo和Fo之间都观察到恒定关系。在SL = 2.0微米时，通过以高达40微米/秒的不同速度进行小的线性长度变化来研究未受刺激肌肉的粘弹性特性。在校正静态平行弹性的贡献后，对拉伸的力响应包括力的指数增加（时间常数τ = 4毫秒）以及拉伸后的指数下降。这种响应符合一个粘性元件与一个弹性元件串联的结构预期。粘性力与拉伸速度成比例增加，在高达15微米/秒时为Fo/微米/秒的0.2 - 0.5%，而计算出的弹性成分的刚度为25 - 45 N·mm-3，这表明这种粘弹性元件最可能的结构候选者是肌联蛋白。500 Hz时的动态刚度与缩短过程中的瞬时力成比例，当在Vo下缩短时，动态刚度是最大单收缩力时刚度的12%。这表明即使在最大激活时，在Vo下缩短过程中主动力产生器的数量也会大幅减少。观察到的Vo和Fo之间的关系可以用一个模型来解释，在该模型中，心肌肌节的缩短速度取决于激活水平，因此取决于支撑粘性负荷的横桥数量。
