Concentration and elongation of attached cross-bridges as pressure determinants in a ventricular model.
Concentration and elongation of attached cross-bridges as pressure determinants in a ventricular model.
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所连接的横桥的浓度和伸长作为心室模型中的压力决定因素。
DOI：
10.1006/jmcc.1999.0984
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发表时间：
1999
影响因子：
5
通讯作者：
E. Lascano
中科院分区：
文献类型：
--
作者：
J. Negroni;E. Lascano
一个心室模型的基础上的肌肉模型肌小节动力学的Ca（2+）动力学，用于建立跨桥动力学的两个组成部分的压力发展的相对贡献：附着的跨桥浓度和其弹性结构的伸长。通过再现反映心室水平肌原纤维行为以及心室机械特性的实验来测试该模型。然后，它被用来研究跨桥行为独立的Ca（2+）激活，通过模拟流钳实验在恒定的Ca（2+）浓度。在量斜坡，减少跨桥伸长率和降低浓度的跨桥分离引起的压力下降;在端喷射有一个快速的部分增加的压力恢复跨桥伸长率，并在后喷射有一个缓慢的压力变化，对端喷射量对应的值，根据钙（2+）动力学常数的速率跨桥再附着。同样，在生理正常射血过程中，结果表明，在模拟搏动中，相对于恒定的跨桥伸长（DeltaP），跨桥伸长（Deltah）的最大减小产生了射血压力的最大减小（DeltaP= 20%，Deltah=17%），以及开胸犬的实验拟合压力-容积数据（DeltaP=43.7+/-3.8%，Deltah=30.7+/-8.3%），Deltah取决于峰值流量（Deltah=0. 1471峰流量+6.0788，r=0.72）。得出结论：正常喷射压力不仅取决于横桥浓度，而且取决于其弹性结构的伸长，该弹性结构根据流量降低压力。
A ventricular model based on a muscle model relating sarcomere dynamics to Ca(2+)kinetics was used to establish the relative contribution to pressure development of the two components of cross-bridge dynamics: attached cross-bridge concentration and elongation of its elastic structure. The model was tested by reproduction of experiments reflecting myofibrillar behavior at the ventricular level as well as chamber mechanical properties. It was then used to study cross-bridge behavior independently of Ca(2+)activation, by simulation of flow-clamp experiments at constant Ca(2+)concentration. During the volume ramp, both reduced cross-bridge elongation and decreased concentration by cross-bridge detachment caused a fall of pressure; at end-ejection there was a fast partial increase of pressure by recovery of cross-bridge elongation, and during post-ejection there was a slower pressure change towards the value corresponding to end-ejection volume by cross-bridge reattachment according to the rate of constants of Ca(2+)kinetics. Likewise, during a physiological normal ejection, results showed that a maximal decrease in cross-bridge elongation (Deltah) produced a maximal reduction of ejecting pressure with respect to that at constant cross-bridge elongation (DeltaP), both in simulated beats (DeltaP=20%, Deltah=17%), and in experimentally fitted pressure-volume data from open-chest dogs (DeltaP=43.7+/-3.8%, Deltah=30.7+/-8.3%), Deltah being dependent of peak flow (Deltah=0. 1471 peak flow+6.0788, r=0.72). We conclude that normal ejecting pressure depends not only on cross-bridge concentration, but also on the elongation of its elastic structure, which reduces pressure according to flow.