AN INTERNAL VISCOUS ELEMENT LIMITS UNLOADED VELOCITY OF SARCOMERE SHORTENING IN RAT MYOCARDIUM
AN INTERNAL VISCOUS ELEMENT LIMITS UNLOADED VELOCITY OF SARCOMERE SHORTENING IN RAT MYOCARDIUM
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DOI：
10.1113/jphysiol.1992.sp019283
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发表时间：
1992-08-01
影响因子：
5.5
通讯作者：
TERKEURS, HEDJ
中科院分区：
文献类型：
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作者：
DETOMBE, PP;TERKEURS, HEDJ
1.从大鼠心脏右心室切下小梁，并在25 ℃下用改良的Krebs-Henseleit溶液灌流，测量小梁的峰值收缩力（F0）和肌节长度（SL）。肌节长度用激光衍射技术测量。用硅树脂应变计测量力。采用等速释放技术测定肌节无负荷缩短速度（V0）.在[Ca 2 +]。= 1.5 mm和SL低于1.9 μ m时，V0与SL成比例增加，而V0与SL高于1.9 μ m无关。在[Ca ~（2+）]o = 0.5 mm时，V0与SL成正比，直至2.2 μ m。在[Ca 2 +]o = 0.2 mm时，V0与SL成比例，最大为2.3 μ m，这是我们能够在我们的小梁中研究的最长SL。在V0和F0之间观察到一种独特的关系，不管F0是否被[Ca 2 +]o或松弛长度以上的肌节长度的变化所改变。被动粘度（F（v））是在1.5 mm [Ca 2 +]o存在下收缩之间的暂停期间，在SL = 2-0-2.1 μ m的范围内，通过以高达v = 30 μ m s-1的各种速度施加0.1 μ m拉伸来测量的。力对拉伸的反应。校正平行弹性力的贡献，显示出粘弹性特征，在拉伸期间指数增加到最大值（F（v）），在拉伸结束后指数下降。当v < 5 μ m s-1时，F（v）增加0.3%F0 μ m-1 s-1;在较高v时，F（v）的增加较小，表明具有非牛顿粘性。5.在拉伸过程中，力增加的时间常数随着v的增加而减少（τ（上升）等于7 ms到τ（上升）等于4 ms）（等于4 μ m s-1到v等于10 μ m s-1; P = 0.02）。拉伸结束时力衰减的时间常数也随着v的增加而减小（τ（衰减）一致-在v一致时为8 ms-到4 μ m s-1-τ（衰减）一致-在v一致时为3 ms-到30 μ m s-1; P < 0-001）。粘弹性元件的弹性项的计算刚度与v无关，即45-50 N mm-3。6.在用无钙Krebs-Henseleit溶液灌注的肌肉中，F（v）略大：在SL = 2.0-2.1-μ-m时，F（v）在[Ca 2 +]时增加0.4%F0-μ-m-1 s-1。= 1.5 mm;在SL = 2.0-2.1 pm的无Ca 2+溶液中，在v < 5-mu-m s-1时，F（v）增加0.53% F0-mu-m-1 s-1。7.动态刚度（DS）被测量为对正弦肌节长度扰动（500 Hz：SL = 11 +/-0.7 nm峰间）的力响应。缩短过程中的动态刚度与载荷（L/F0）成正比，拟合方程为：DS = 12.0 + 0.084L/F0（r = 0.84）。另一方面，相移（PHI）与L无关：PHI = 51.8 + 0.05L（r = 0.01）。根据观测到的DS和L/F0之间的关系，计算出的一座横桥的力-速度关系接近线性，正如Huxley（1957）模型所预测的那样。这些结果进行了讨论的模型，其中卸载的心脏肌节的缩短速度是有限的被动粘度的肌肉。该模型充分预测了观察到的V0和F0之间的关系。
1. Peak twitch force (F0) and sarcomere length (SL) were measured in trabeculae that had been dissected from the right ventricle of rat heart and that were superfused with a modified Krebs-Henseleit solution at 25-degrees-C. Sarcomere length was measured by laser diffraction techniques. Force was measured with a silicone strain gauge. Unloaded velocity of sarcomere shortening (V0) was measured by the 'isovelocity release' technique.2. At [Ca2+]. = 1.5 mm and SL below 1.9-mu-m, V0 increased in proportion to SL, while V0 was independent of SL above 1.9-mu-m. At [Ca2+]o = 0.5 mm, V0 was proportional to SL up to 2.2-mu-m. At [Ca2+]o = 0.2 mm. V0 was proportional to SL up to 2.3-mu-m which is the longest SL that we were able to study in our trabeculae.3. A unique relationship was observed between V0 and F0, irrespective of whether F0 was altered by variation of [Ca2+]o or sarcomere length above slack length.4. Passive viscosity (F(v)) was measured during the pause between contractions in the presence of 1.5 mm [Ca2+]o and in the range SL = 2-0-2.1-mu-m by applying 0.1-mu-m stretches at various velocities up to v = 30-mu-m s-1. The force response to stretch. corrected for the contribution of parallel elastic force, showed viscoelastic characteristics with an exponential increase to a maximum (F(v)) during stretch and an exponential decline after the end of the stretch. F(v) increased, by 0.3 % F0-mu-m-1 s-1, in proportion to v < 5-mu-m s-1; the increase of F(v) was smaller at higher v, suggesting non-Newtonian viscous properties. 5. The time constant of the increase of force during the stretch decreased (tau(rise) congruent-to 7 ms to tau(rise) congruent-to 4 ms) with increases in v ( congruent-to 4-mu-m s-1 to v congruent-to 10-mu-m s-1; P = 0.02). The time constant of decay of force at the end of the stretch also decreased with increases in v (tau(decay) congruent-to 8 ms at v congruent-to 4-mu-m s-1 to tau(decay) congruent-to 3 ms at v congruent-to 30-mu-m s-1; P < 0-001). Calculated stiffness of the elastic term of the viscoelastic element was independent of v, i.e. 45-50 N mm-3. 6. F(v) was slightly larger in muscles that were superfused with Ca2+-free Krebs-Henseleit solution: at SL = 2.0-2.1-mu-m, F(v) increased by 0.4 % F0-mu-m-1 s-1 at [Ca2+]. = 1.5 mm; at SL = 2.0-2.1 pm in Ca2+-free solution, F(v) increased by 0.53 % F0-mu-m-1 s-1 at v < 5-mu-m s-1. 7. Dynamic stiffness (DS) was measured as the force response to sinusoidal sarcomere length perturbations (500 Hz: SL = 11 +/- 0.7 nm peak to peak). Dynamic stiffness during shortening was proportional to the load (L/F0) and was fitted to: DS = 12.0 + 0.084L/F0 (r = 0.84). The phase shift (PHI) on the other hand, was independent of L: PHI = 51.8 + 0.05L (r = 0.01).8. The force-velocity relation calculated for one crossbridge on the basis of the observed relationship between DS and L/F0 was close to linear, as is predicted by Huxley's (1957) model.9. These results are discussed in relation to a model in which the unloaded shortening velocity of the cardiac sarcomere is limited by the passive viscosity of the muscle. The model adequately predicts the observed relation between V0 and F0.