P13-12 Relationship between mechanomyographic activity and muscle length during single twitch contraction

2010 ◽  
Vol 121 ◽  
pp. S181
Author(s):  
M. Takesada ◽  
K. Akataki ◽  
Y. Itoh ◽  
K. Mita ◽  
T. Sato ◽  
...  
1999 ◽  
Vol 276 (1) ◽  
pp. H289-H299 ◽  
Author(s):  
Tetsuya Ishikawa ◽  
Hidetoshi Kajiwara ◽  
Satoshi Kurihara

We investigated the contribution of sarcoplasmic reticulum (SR) and Na+/Ca2+exchanger in the tension-dependent change in the decay of the Ca2+ transients (CaT) in euthyroid (Eu) and hyperthyroid (Hy) myocardium. Hy was induced by thyroxine treatment to enhance the rate of SR Ca2+ uptake. With the use of the aequorin method, CaT and tension in twitch contraction were simultaneously measured under various conditions (changing muscle length and Ca2+ concentration in solution). In both groups, the decay time of CaT (DT) showed a significant dependence on the developed tension, but the tension dependence of DT in Hy was significantly less than in Eu. In the presence of caffeine (3 mM), the tension dependence of DT in Hy became apparent as in Eu. Inhibition of Na+/Ca2+exchanger by replacing Na+ with Li+ did not affect the dependence in Hy. The normalized extra Ca2+, which is the Ca2+ concentration change in response to a quick length change, in Hy was similar to that in Eu. pCa-tension relations of skinned trabeculae measured at different lengths (1.9 and 2.3 μm) were nearly identical in both groups. These results indicate that the tension-dependent change in the affinity of troponin C for Ca2+works in both Eu and Hy myocardium and that the tension-dependent change in DT is influenced by the Ca2+ uptake rate of SR.


1996 ◽  
Vol 270 (4) ◽  
pp. H1501-H1508 ◽  
Author(s):  
H. Yamaguchi ◽  
M. Takaki ◽  
H. Matsubara ◽  
S. Yasuhara ◽  
H. Suga

We simulated myocardial Ca2+ (Ca) and cross-bridge (CB) kinetics to get insight into the experimentally observed constancy and variability of cardiac contractile efficiency in generating total mechanical energy under various inotropic and pathological conditions. The simulation consisted of a Ca transient, Ca association and dissociation rate constants of troponin C, and CB on and off rate constants. We evaluated sarcomere isometric twitch contractions at a constant muscle length. We assumed that each CB cycle hydrolyzes one ATP and that the force-length area (FLA) quantifies the total mechanical energy generated by CB cycles in a twitch contraction. FLA is a linear version of pressure-volume area, which quantifies the total mechanical energy of cardiac twitch contraction and correlates linearly with cardiac oxygen consumption (H. Suga, Physiol. Rev. 70: 247-277, 1990). The simulation shows that the contractile efficiency varies with changes in the Ca transient and Ca and CB kinetics except when they simultaneously speed up or slow down proportionally. These results point to possible mechanisms underlying the constancy and variability of cardiac contractile efficiency.


1998 ◽  
Vol 274 (1) ◽  
pp. H147-H154 ◽  
Author(s):  
Kimiaki Komukai ◽  
Tetsuya Ishikawa ◽  
Satoshi Kurihara

We investigated the effects of acidosis on the intracellular Ca2+ concentration ([Ca2+]i) and contractile properties of intact mammalian cardiac muscle during tetanic and twitch contractions. Aequorin was injected into ferret papillary muscles, and the [Ca2+]iand tension were simultaneously measured. Acidosis was attained by increasing the CO2 concentration in the bicarbonate (20 mM)-buffered Tyrode solution from 5% (pH 7.35, control) to 15% (pH 6.89, acidosis). Tetanic contraction was produced by repetitive stimulation of the preparation following treatment with 5 μM ryanodine. The relationship between [Ca2+]iand tension was measured 6 s after the onset of the stimulation and was fitted using the Hill equation. Acidosis decreased the maximal tension to 81 ± 2% of the control and shifted the [Ca2+]i-tension relationship to the right by 0.18 ± 0.01 pCa units. During twitch contraction, a quick shortening of muscle length from the length at which developed tension became maximal ( L max) to 92% L maxproduced a transient change in the [Ca2+]i(extra Ca2+). The magnitude of the extra Ca2+ was dependent on the [Ca2+]iimmediately before the length change, suggesting that the extra Ca2+ is related to the amount of troponin-Ca complex. Acidosis decreased the normalized extra Ca2+ to [Ca2+]iimmediately before the length change, which indicates that the amount of Ca2+ bound to troponin C is less when [Ca2+]iis the same as in the control. The decrease in the Ca2+ binding to troponin C explains the decrease in tetanic and twitch contraction, and mechanical stress applied to the preparation induced less [Ca2+]ichange in acidosis.


1966 ◽  
Vol 49 (3) ◽  
pp. 517-535 ◽  
Author(s):  
C. L. Gibbs ◽  
N. V. Ricchiuti ◽  
W. F. H. M. Mommaerts

Upon excitation of a muscle with two stimuli and variation of the interval between them up to the end of the period of full mechanical fusion, an increment of the isometric heat over that found in a single twitch is obtained. This is a good approximation to the activation heat, directly at 0°C, or after certain corrections which become important at higher temperature. The activation heat so found is independent of the muscle length and nearly independent of temperature. It is increased by nitrate and caffeine.


2001 ◽  
Vol 79 (1) ◽  
pp. 68-72 ◽  
Author(s):  
Masahito Miura ◽  
Yuji Wakayama ◽  
Yoshinao Sugai ◽  
Yutaka Kagaya ◽  
Jun Watanabe ◽  
...  

Transient stretch of cardiac muscle during a twitch contraction may dissociate Ca2+ from myofilaments into the cytosol at the moment of quick release of the muscle. We studied the effect of stretch and quick release of trabeculae on changes in intracellular Ca2+ ([Ca2+]i) during triggered propagated contractions (TPCs). Trabeculae were dissected from the right ventricle of 9 rat hearts. [Ca2+]i was measured using electrophoretically injected fura-2. Force was measured using a silicon strain gauge and sarcomere length was measured using laser diffraction techniques. Reproducible TPCs (n = 13) were induced by trains of electrical stimuli (378 ± 19 ms interval) for 7.5 s at [Ca2+]o of 2.0 mM (27.9 ± 0.2°C). The latency of the TPC force and the underlying increase in [Ca2+]i was calculated from the time (TimeF) between the last stimulus and the peak of TPC force (PeakF), or the time (TimeCa) between the last stimulus and the peak of the increase in [Ca2+]i during the TPCs (PeakCa). As a result of a 10% increase in muscle length for 150-200 ms during the last stimulated twitches, TimeF and TimeCa decreased and PeakF and PeakCa increased significantly (n = 13). In addition, transient stretch sometimes induced a twitch contraction subsequent to the accelerated TPC and its underlying increase in [Ca2+]i. These results suggest that Ca2+ binding and dissociation from the myofilaments by the stretch and quick release of muscle may modulate the TPC force and the underlying increases in [Ca2+]i and play an important role in the induction of arrhythmias.Key words: rat cardiac trabeculae, stretch, calcium transients.


Author(s):  
G.E. Adomian ◽  
L. Chuck ◽  
W.W. Pannley

Sonnenblick, et al, have shown that sarcomeres change length as a function of cardiac muscle length along the ascending portion of the length-tension curve. This allows the contractile force to be expressed as a direct function of sarcomere length. Below L max, muscle length is directly related to sarcomere length at lengths greater than 85% of optimum. However, beyond the apex of the tension-length curve, i.e. L max, a disparity occurs between cardiac muscle length and sarcomere length. To account for this disproportionate increase in muscle length as sarcomere length remains relatively stable, the concept of fiber slippage was suggested as a plausible explanation. These observations have subsequently been extended to the intact ventricle.


1986 ◽  
Vol 65 (Supplement 3A) ◽  
pp. A199 ◽  
Author(s):  
M. E. Goldberg ◽  
C. Gregg ◽  
A. T. Marr ◽  
G. E. Larijani ◽  
J. L. Seltzer
Keyword(s):  

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