ter Keurs H E, Bucx J J, de Tombe P P, Backx P, Iwazumi T
Department of Medicine, University of Calgary, AB, Canada.
Adv Exp Med Biol. 1988;226:581-93.
The mechanism(s) underlying the effects of varied calcium concentration and of varied sarcomere length on force development and on the velocity of shortening in cardiac muscle were investigated. Sarcomere dynamics were investigated in thin trabeculae from rat heart with laser diffraction techniques; force was measured with silicon strain gauge 10 kHz. The unloaded velocity of sarcomere shortening was measured with the use of the 'isovelocity' technique. After study of intact muscles, superfused with modified Krebs-Henseleit solution at 25 degrees C, preparations were skinned with relaxing solution containing Triton X-100 and investigated at varied free Ca++. Force increased in all intact muscles continually with sarcomere length from 1.6-2.4 microns; the relation between force and sarcomere length was convex toward the ordinate at high Ca++0 and convex toward the abscissa at low Ca++0. Similar relations between force and sarcomere length were found in skinned trabeculae. Unloaded velocity of shortening (V0) was independent of time between 50 ms and 150 ms following onset of the twitch. V0 increased, in this period with increasing sarcomere length from 1.6 to 1.9 microns from 0 to 13 micron/s; above that length the velocity was constant. V0 increased at a sarcomere length of 2.00 microns with increasing Ca++0 to a maximum at Ca++0 = 1.2 mM above which V0 remained constant though force increased by 100%. These results suggest that the force-sarcomere length relation in cardiac muscle can be explained on the basis of length dependent activation of the contractile filaments to Ca++. Whether the different responses of force and of unloaded velocity of shortening to variations in sarcomere length and in Ca++ concentration are consistent with the hypothesis that force development and unloaded velocity of shortening are controlled by different mechanisms is discussed.
研究了不同钙浓度和不同肌节长度对心肌力量发展和缩短速度的影响机制。采用激光衍射技术研究了大鼠心脏细小梁中的肌节动力学；用硅应变片在10kHz频率下测量力量。采用“等速”技术测量肌节缩短的无负荷速度。在25℃下用改良的克雷布斯-亨泽莱特溶液对完整肌肉进行灌流研究后，用含有 Triton X-100的松弛溶液对标本进行透皮处理，并在不同的游离钙离子浓度下进行研究。所有完整肌肉中的力量随着肌节长度从1.6 - 2.4微米不断增加；在高钙离子浓度时，力量与肌节长度的关系向纵坐标凸出，在低钙离子浓度时向横坐标凸出。在透皮小梁中也发现了力量与肌节长度之间的类似关系。在抽搐开始后的50毫秒至150毫秒之间，缩短的无负荷速度（V0）与时间无关。在此期间，随着肌节长度从1.6微米增加到1.9微米，V0从0增加到13微米/秒；超过该长度后速度保持恒定。在肌节长度为2.00微米时，V0随着钙离子浓度增加而增加，在钙离子浓度为1.2 mM时达到最大值，超过此值后V0保持恒定，尽管力量增加了100%。这些结果表明，心肌中力量 - 肌节长度关系可以基于收缩细丝对钙离子的长度依赖性激活来解释。讨论了力量和缩短的无负荷速度对肌节长度和钙离子浓度变化的不同反应是否与力量发展和缩短的无负荷速度由不同机制控制的假设一致。
