scholarly journals The static preload associated myogenic spontaneous fasciculation response in lengthening cardiac muscle

2021 ◽  
Author(s):  
Shouyan Fan ◽  
Lingfeng Gao ◽  
Annie Christel Bell ◽  
Joseph Akparibila Azure ◽  
Yang Wang
Keyword(s):  
Cardiac Muscle ◽  
Passive Tension ◽  
Force Enhancement ◽  
Static Stretch ◽  
Time Integral ◽  
Physiological Properties ◽  
Intracellular Ca ◽  
Tension Time ◽  
Cardiac Relaxation ◽  
Contraction Cycle

Abstract The passive tension force enhancement is one kind of myogenic spontaneous fasciculation in muscles. However, its physiological properties in cardiac fibres are not well known. In this study, mice cardiac papillary muscle spontaneous force enhancement was evaluated by micro stepping stretch method. The occurrence of spontaneous force and real time cardiac fibre Ca2+ redistribution was tranced by Flou-3 (2mM) indicator. Force enhancement amplitude, enhancement prolonging time, and tension–time integral were analysis by myograph analyser. The results indicated that the spontaneous force occurred immediately after the active stretch, rapidly enhanced during tolerating the sustained static stretch. The force occurrence and amplitude enhance synchronized with the Ca2+ recruitment and lightning transmitted to adjacent fibres. In high preload fibres, the enhancement was forceful to over its maximum passive tension (6.20 ± 0.51 N/mm2 to 4.49 ± 0.43 N/mm2). The force occurrences were unsteadiness in each stretch. The increased enhancement amplitude combining with the shortening prolonging time induced reduction of tension–time integral. We concluded that the intracellular Ca2+ synchronized force enhancement is one kind of interruption event in overloading cardiac fibres. This interruption occurred during the relaxation processing in cardiac muscle, therefore affect the rhythmic stability of cardiac relaxation-contraction cycle.

scholarly journals Spontaneous myogenic fasciculation associated with the lengthening of cardiac muscle in response to static preloading

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shouyan Fan ◽  
Lingfeng Gao ◽  
Annie Christel Bell ◽  
Joseph Akparibila Azure ◽  
Yang Wang
Keyword(s):  
Cardiac Muscle ◽  
Striated Muscles ◽  
Force Enhancement ◽  
Static Stretch ◽  
Relaxation Period ◽  
Time Integral ◽  
Intracellular Ca ◽  
Tension Time ◽  
Cardiac Relaxation

AbstractForce enhancement is one kind of myogenic spontaneous fasciculation in lengthening preload striated muscles. In cardiac muscle, the role of this biomechanical event is not well established. The physiological passive property is an essential part for maintaining normal diastole in the heart. In excessive preload heart, force enhancement relative erratic passive properties may cause muscle decompensating, implicate in the development of diastolic dysfunction. In this study, the force enhancement occurrence in mouse cardiac papillary muscle was evaluated by a microstepping stretch method. The intracellular Ca2+ redistribution during occurrence of force enhancement was monitored in real-time by a Flou-3 (2 mM) indicator. The force enhancement amplitude, the enhancement of the prolongation time, and the tension–time integral were analyzed by myography. The results indicated that the force enhancement occurred immediately after active stretching and was rapidly enhanced during sustained static stretch. The presence of the force and the increase in the amplitude synchronized with the acquisition and immediate transfer of Ca2+ to adjacent fibres. In highly preloaded fibres, the enhancement exceeded the maximum passive tension (from 4.49 ± 0.43 N/mm2 to 6.20 ± 0.51 N/mm2). The occurrence of force enhancement were unstable in each static stretch. The increased enhancement amplitude combined with the reduced prolongation time to induce a reduction in the tension–time integral. We concluded that intracellular Ca2+-synchronized force enhancement is one kind of interruption event in excessive preload cardiac muscle. During the cardiac muscle in its passive relaxation period, the occurrence of this interruption affected the rhythmic stability of the cardiac relaxation cycle.

scholarly journals An analysis of the effects of stretch on IGF-I secretion from rat ventricular fibroblasts

2007 ◽  
Vol 293 (1) ◽  
pp. H677-H683 ◽  
Author(s):  
Betty S. Hu ◽  
Lee K. Landeen ◽  
Nakon Aroonsakool ◽  
Wayne R. Giles
Keyword(s):  
Cardiac Fibroblasts ◽  
Cyclic Stretch ◽  
Dependent Manner ◽  
Paracrine Factor ◽  
Static Stretch ◽  
Paracrine Factors ◽  
Adult Rat ◽  
Igf I ◽  
Intracellular Ca ◽  
Altered Gene

Mechanical force can induce a number of fundamental short- and long-term responses in myocardium. These include alterations in ECM, activation of cell-signaling pathways, altered gene regulation, changes in cell proliferation and growth, and secretion of a number of peptides and growth factors. It is now known that a number of these autocrine/paracrine factors are secreted from both cardiomyocytes and ventricular cardiac fibroblasts (CFb) in response to stretch. One such substance is IGF-I. IGF-I is an important autocrine/paracrine factor that can regulate physiological or pathophysiological responses, such as hypertrophy. In this study, we addressed the possible effects of mechanical perturbation, biaxial strain, on IGF-I secretion from adult rat CFb. CFb were subjected to either static stretch (3–10%) or cyclic stretch (10%; 0.1–1 Hz) over a 24-h period. IGF-1 secretion from CFb in response to selected stretch paradigms was examined using ELISA to measure IGF-I concentrations in conditioned media. Static stretch did not result in any measurable modulation of IGF-I secretion from CFb. However, cyclic stretch significantly increased IGF-I secretion from CFb in a frequency- and time-dependent manner compared with nonstretched controls. This stretch-induced increase in secretion was relatively insensitive to changes in extracellular [Ca2+] or to block of L-type Ca2+ channels. In contrast, thapsigargin, an inhibitor of sarco(endo)plasmic reticulum Ca2+ ATPase, remarkably decreased stretch-induced IGF-I secretion from CFb. We further show that IGF-I can upregulate mRNA expression of atrial natriuretic peptide in myocytes. In summary, cyclic stretch can significantly increase IGF-I secretion from CFb, and this effect is dependent on a thapsigargin-sensitive pool of intracellular [Ca2+].

Regulation of energy consumption in cardiac muscle: analysis of isometric contractions

1999 ◽  
Vol 276 (3) ◽  
pp. H998-H1011 ◽  
Author(s):  
Amir Landesberg ◽  
Samuel Sideman
Keyword(s):  
Energy Consumption ◽  
Cardiac Muscle ◽  
Feedback Mechanism ◽  
Isometric Contractions ◽  
Cross Bridge ◽  
Time Integral ◽  
Length Relationship ◽  
Cross Bridges ◽  
Force Time ◽  
Force Time Integral

The well-known linear relationship between oxygen consumption and force-length area or the force-time integral is analyzed here for isometric contractions. The analysis, which is based on a biochemical model that couples calcium kinetics with cross-bridge cycling, indicates that the change in the number of force-generating cross bridges with the change in the sarcomere length depends on the force generated by the cross bridges. This positive-feedback phenomenon is consistent with our reported cooperativity mechanism, whereby the affinity of the troponin for calcium and, hence, cross-bridge recruitment depends on the number of force-generating cross bridges. Moreover, it is demonstrated that a model that does not include a feedback mechanism cannot describe the dependence of energy consumption on the loading conditions. The cooperativity mechanism, which has been shown to determine the force-length relationship and the related Frank-Starling law, is shown here to provide the basis for the regulation of energy consumption in the cardiac muscle.

Voltage-independent changes in L-type Ca2+current uncoupled from SR Ca2+ release in cardiac myocytes

2000 ◽  
Vol 279 (4) ◽  
pp. H2024-H2031 ◽  
Author(s):  
Andrzej M. Janczewski ◽  
Edward G. Lakatta ◽  
Michael D. Stern
Keyword(s):  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Abrupt Increase ◽  
Time To Peak ◽  
Time Integral ◽  
Marked Disparity ◽  
Release Flux ◽  
Intracellular Ca ◽  
Combined Actions ◽  
Continuous Presence

To determine the effect of voltage-independent alterations of L-type Ca2+ current ( I Ca) on the sarcoplasmic reticular (SR) Ca2+ release in cardiac myocytes, we measured I Ca and cytosolic Ca2+ transients (Cai 2+; intracellular Ca2+ concentration) in voltage-clamped rat ventricular myocytes during 1) an abrupt increase of extracellular [Ca2+] (Cao 2+) or 2) application of 1 μM FPL-64176, a Ca2+channel agonist, to selectively alter I Ca in the absence of changes in SR Ca2+ loading. On the first depolarization in higher Cao 2+, peak I Ca was increased by 46 ± 6% ( P < 0.001), but the increases in the maximal rate of rise of Cai 2+(dCai 2+/d t max, where t is time; an index of SR Ca2+ release flux) and the Cai 2+ transient amplitude were not significant. Rapid exposure to FPL-64176 greatly slowed inactivation of I Ca, increasing its time integral by 117 ± 8% ( P < 0.001) without significantly increasing peak I Ca, dCai 2+/d t max, or amplitude of the corresponding Cai 2+ transient. Prolongation of exposure to higher Cao 2+ or FPL-64176 did not further increase peak I Ca but greatly increased dCai 2+/d t max, Cai 2+ transient amplitude, and the gain of Ca2+ release (dCai 2+/d t max/ I Ca), evidently due to augmentation of the SR Ca2+ loading. Also, the time to peak dCai 2+/d t maxwas significantly increased in the continuous presence of higher Cao 2+ (by 37 ± 5%, P < 0.001) or FPL-64176 (by 63 ± 5%, P < 0.002). Our experiments provide the first evidence of a marked disparity between an increased peak I Ca and the corresponding SR Ca2+ release. We attribute this to saturation of the SR Ca2+ release flux as predicted by local control theory. Prolongation of the SR Ca2+ release flux, caused by combined actions of a larger I Ca and maximally augmented SR Ca2+ loading, might reflect additional Ca2+ release from corbular SR.

Calcium binding to cardiac sarcolemmal vesicles: potential role as a modifier of contraction

1986 ◽  
Vol 251 (6) ◽  
pp. C861-C871 ◽  
Author(s):  
D. M. Bers ◽  
L. A. Allen ◽  
Y. Kim
Keyword(s):  
Membrane Potential ◽  
Muscle Contraction ◽  
Cardiac Muscle ◽  
Calcium Binding ◽  
Potential Role ◽  
Cardiac Contractile ◽  
Inner Surface ◽  
Intracellular Ca ◽  
Sarcolemmal Vesicles ◽  
Contractile Performance

Passive Ca binding to cardiac sarcolemmal vesicles isolated from rabbit ventricles was measured under ionic conditions similar to intracellular and extracellular media. The first of two main goals was to evaluate whether certain agents induce changes in Ca binding at the external sarcolemmal surface that might contribute to the overall effect of these agents on cardiac muscle contraction. The agents studied were ouabain, verapamil, nifedipine, Bay K 8644, caffeine, ryanodine, and milrinone over a broad range of concentrations, including concentrations at which these agents exert strong effects on cardiac contractile performance. None of these agents produced significant alterations in Ca binding, such that it is unlikely that any part of their actions can be attributed to changes in Ca binding to the external sarcolemmal surface. In contrast, when [Na] is reduced from 140 mM, sarcolemmal Ca binding increases or decreases depending on what replacement is used to avoid changes of osmolarity. Thus the possible effect of Na reduction on surface Ca must be considered in physiological experiments where extracellular [Na] is changed. The second main goal was to evaluate the effects of membrane potential, Na and Mg on Ca bound to the inner surface of the sarcolemma under ionic conditions similar to those expected intracellularly (e.g., [Ca] = 0.3-5.0 microM). Ca binding was inhibited by physiological concentrations of Na and Mg and was sensitive to membrane potential such that depolarization of a normally polarized cell would cause Ca to be released from these sarcolemmal sites. From a quantitative standpoint, it is not clear whether the effect of depolarization would be to contribute sarcolemmal Ca to the activation of the myofilaments or merely to limit the ability of the inner sarcolemmal surface to buffer the rise in intracellular [Ca] associated with contraction.

Rapid dilation of arterioles with single contraction of hamster skeletal muscle

2006 ◽  
Vol 290 (1) ◽  
pp. H119-H127 ◽  
Author(s):  
Jurgen W. G. E. VanTeeffelen ◽  
Steven S. Segal
Keyword(s):  
Skeletal Muscle ◽  
Muscarinic Receptor ◽  
Muscle Blood Flow ◽  
Rapid Onset ◽  
Receptor Activation ◽  
Retractor Muscle ◽  
Time Integral ◽  
Exercise Onset ◽  
Tension Time ◽  
Motor End Plates

Skeletal muscle blood flow increases rapidly with exercise onset, but little is known of where or how the rapid onset of vasodilation (ROV) is governed within the microcirculation. In the retractor muscle of anesthetized hamsters ( n = 26), we tested the following: 1) where in the resistance network ROV occurred, 2) how microvascular responses were affected by the duration of contraction, and 3) whether ROV involved muscarinic receptor activation. Single tetanic contractions were evoked using supramaximal field stimulation (100 Hz) to depolarize motor end plates. In response to a 200-ms contraction, red blood cell (rbc) velocity ( Vrbc) in feed arteries (FA; rest: 17.8 ± 2 mm/s) increased within 1 s; a transient first peak (P1; 50 ± 7% increase) occurred at ∼5 s; and a second peak (P2; 50 ± 15% increase) occurred at ∼15–20 s. For vasodilation, P1 increased in frequency from proximal FA (2/7) and 1A arterioles (2/7) to distal 2A (4/7) and 3A (7/8) arterioles ( P < 0.05). Relative to resting (and maximal, 10 μM sodium nitroprusside) diameters, P1 increased from proximal (FA, 3 ± 2% from 57 ± 5 μm) to distal (3A, 27 ± 6% from 14 ± 1 μm) vessel branches ( P < 0.05). P2 was manifest in all vessels and increased relative to resting diameters from FA (11 ± 3%) to 3A (36 ± 6%) branches ( P < 0.01). Extending a contraction from 200 to 1,000 ms (tension × time integral from 17 ± 2 to 73 ± 4 mN/mm2 × s) increased P1 and P2 for Vrbc and for diameter ( P < 0.05) while reducing the time of onset for P2 ( P < 0.05). Superfusion with atropine (10 μM) attenuated P1 of vasodilation (200 ms contraction) from 26 ± 8% to 6 ± 2% ( n = 7 across branches; P < 0.05) and reduced the diameter × time integral by 46 ± 13% ( P < 0.05) without changing P2. We conclude that ROV in the hamster retractor muscle is initiated in distal arterioles, increases with the duration of muscle contraction, and involves muscarinic receptor activation.

Comparison of the cardiac force-time integral with energetics using a cardiac muscle model

1993 ◽  
Vol 26 (10) ◽  
pp. 1217-1225 ◽  
Author(s):  
Tad W. Taylor ◽  
Yoichi Goto ◽  
Katsuya Hata ◽  
Toshiyuki Takasago ◽  
Akio Saeki ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Muscle Model ◽  
Time Integral ◽  
Force Time ◽  
Force Time Integral

Mechanical work, oxygen consumption, and efficiency in isolated frog and rat muscle

1987 ◽  
Vol 253 (1) ◽  
pp. C22-C29 ◽  
Author(s):  
N. C. Heglund ◽  
G. A. Cavagna
Keyword(s):  
Oxygen Consumption ◽  
Rana Esculenta ◽  
Time Integral ◽  
Wistar Strain ◽  
Measured Efficiency ◽  
Tension Time ◽  
Second Procedure ◽  
Work Done ◽  
Positive Work

The total work done during shortening, in repeated stretch-shortening cycles and the subsequent recovery oxygen consumption were measured in isolated frog (Rana esculenta) sartorius at 12 degrees C and rat (Wistar strain) extensor digitorum longus (EDL) and soleus at 20 degrees C. Two procedures were followed. In the first, the muscles were lengthened in the relaxed state and stimulated isometrically just before and during the first part of shortening. The peak efficiency (positive work done divided by the energetic equivalent of the oxygen consumed) was approximately 25% at 0.75–1.5 muscle lengths/s (Lo/s) in sartorius, 19% at 1.0 Lo/s in EDL, and 15% at 0.5 Lo/s in the soleus. In contrast to the measured efficiency values, the ratio between the tension-time integral and the oxygen consumption (the economy) is greater in soleus than in EDL. In the second procedure, stimulation began before stretching and continued during the first part of shortening. In this case, the efficiency attained values of approximately 35% in sartorius, 50% in EDL, and 40% in soleus. These values are in rough agreement with those measured in vivo during running.

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