FORCE, NOT SARCOMERE-LENGTH, CORRELATES WITH PROLONGATION OF ISOSARCOMETRIC CONTRACTION
FORCE, NOT SARCOMERE-LENGTH, CORRELATES WITH PROLONGATION OF ISOSARCOMETRIC CONTRACTION
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DOI：
10.1152/ajpheart.1995.269.2.h676
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发表时间：
1995-08-01
影响因子：
4.8
通讯作者：
HUNTER, WC
中科院分区：
文献类型：
--
作者：
JANSSEN, PML;HUNTER, WC
最近的研究强调了收缩晚期对于理解心室射血的重要性。为了研究控制这一阶段的心肌因素，我们研究了9个离体大鼠小梁收缩收缩的时间。通过改变肌节长度（SL）和细胞外Ca 2+浓度（[Ca 2 +]），我们确定了这些因素中的哪一个或开发的峰值抽搐力更好地与收缩的延长相关。我们关注的是从力的峰值之前到半弛豫的时间段。SL通过激光衍射测量，并使用自适应控制保持恒定。峰值收缩力是与收缩延长最密切相关的因素：当力从10 mN/mm（2）增加到100 mN/mm（2）时，持续时间从100 ms增加到300 ms。然而，当力的趋势被移除时，SL的单独影响没有保留。[Ca 2 +]（0）缩短收缩的增加在所有力水平下均相等。收缩晚期收缩的延长也与晚期松弛的时间常数的延长高度相关，这表明峰值抽搐力延长抽搐的整个后续时间过程的共同机制。我们假设1）增加的力与延长的Ca 2+与肌钙蛋白C的结合相关，和/或2）连接的横桥协同作用，以对抗原肌球蛋白的抑制作用，因为Ca 2+从细丝中丢失。
Recent studies have emphasized the importance of the late systolic phase for understanding ventricular ejection. To examine the myocardial factors controlling this phase, we studied the timing of twitch contraction in nine excised rat trabeculae contracting isosarcometrically. By varying both sarcomere length (SL) and extracellular Ca2+ concentration ([Ca2+],) we determined which of these factors or the developed peak twitch force correlated better with the prolongation of contraction. We focused on the period from just before the peak of force to the time of half relaxation. SL was measured by laser diffraction and kept constant using adaptive control. Peak twitch force was the factor most tightly correlated with prolongation of contraction: as force rose from 10 to 100 mN/mm(2), duration tripled from 100 to 300 ms. When the trend with force was removed, however, no separate influence of SL remained. Increase in [Ca2+](0) abbreviated contraction equally at all force levels. Prolongation of late systolic contraction was also highly correlated with prolongation of the time constant for late relaxation, suggesting a common mechanism by which peak twitch force lengthens the entire subsequent time course of a twitch. We hypothesize that 1) increased force correlates with prolonged Ca2+ binding to troponin-C, and/or 2) attached cross bridges act cooperatively to oppose the inhibiting effects of tropomyosin as Ca2+ is lost from the thin filaments.