scholarly journals Stretch and quick release of rat cardiac trabeculae accelerates Ca2+ waves and triggered propagated contractions

2001 ◽  
Vol 281 (5) ◽  
pp. H2133-H2142 ◽  
Author(s):  
Yuji Wakayama ◽  
Masahito Miura ◽  
Yoshinao Sugai ◽  
Yutaka Kagaya ◽  
Jun Watanabe ◽  
...  
Keyword(s):  
Strain Gauge ◽  
Sarcomere Length ◽  
Muscle Length ◽  
Laser Diffraction ◽  
Active Force ◽  
Quick Release ◽  
Rat Hearts ◽  
Initiation And Propagation ◽  
Intracellular Ca ◽  
Ventricular Trabeculae

Rapid shortening of active cardiac muscle [quick release (QR)] dissociates Ca2+ from myofilaments. We studied, using muscle stretches and QR, whether Ca2+ dissociation affects triggered propagated contractions (TPCs) and Ca2+waves. The intracellular Ca2+ concentration was measured by a SIT camera in right ventricular trabeculae dissected from rat hearts loaded with fura 2 salt, force was measured by a silicon strain gauge, and sarcomere length was measured by laser diffraction while a servomotor controlled muscle length. TPCs ( n = 27) were induced at 28°C by stimulus trains (7.5 s at 2.65 ± 0.13 Hz) at an extracellular Ca2+ concentration ([Ca2+]o) = 2.0 mM or with 10 μM Gd3+ at [Ca2+]o = 5.2 ± 0.73 mM. QR during twitch relaxation after a 10% stretch for 100–200 ms reduced both the time between the last stimulus and the peak TPC (PeakTPC) and the time between the last stimulus and peak Ca2+ wave (PeakCW) and increased PeakTPC and PeakCW ( n= 13) as well as the propagation velocity ( V prop; n = 8). Active force during stretch also increased V prop( r = 0.84, n = 12, P < 0.01), but Gd3+ had no effect ( n = 5). These results suggest that Ca2+ dissociation by QR during relaxation accelerates the initiation and propagation of Ca2+ waves.

Effect of transient stretch on intracellular Ca2+ during triggered propagated contractions in intact trabeculae

2001 ◽  
Vol 79 (1) ◽  
pp. 68-72 ◽  
Author(s):  
Masahito Miura ◽  
Yuji Wakayama ◽  
Yoshinao Sugai ◽  
Yutaka Kagaya ◽  
Jun Watanabe ◽  
...  
Keyword(s):  
Sarcomere Length ◽  
Muscle Length ◽  
Twitch Contraction ◽  
Quick Release ◽  
Rat Hearts ◽  
Force Peak ◽  
Intracellular Ca ◽  
The Moment ◽  
The Right ◽  
Electrical Stimuli

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.

Unstimulated force during hypoxia of rat cardiac muscle: stiffness and calcium dependence

1990 ◽  
Vol 258 (3) ◽  
pp. H861-H869 ◽  
Author(s):  
W. J. Leijendekker ◽  
W. D. Gao ◽  
H. E. ter Keurs
Keyword(s):  
Oxidative Phosphorylation ◽  
Strain Gauge ◽  
Sarcomere Length ◽  
Muscle Length ◽  
Laser Diffraction ◽  
Muscle Stiffness ◽  
Rapid Cycling ◽  
Cross Bridges ◽  
Passive Muscle

The stiffness of rat cardiac trabeculae was measured in vitro to distinguish between an increase in unstimulated force (Fu) caused by rapid cycling of cross bridges or caused by rigor bridges during hypoxia. The force was measured with a strain gauge, the sarcomere length was determined by laser diffraction techniques, and muscle length was controlled by means of a motor. Stiffness was analyzed by using small (less than 1% of muscle length) sinusoidal length perturbations of 1 and 100 Hz. The stiffness at 100 Hz increased linearly with force during tetani at a varied [Sr2+] (0.25-10 mM) in the Krebs-Henseleit (K-H) buffer, but remained virtually unchanged at 1 Hz. In contrast, the stiffness of both the passive muscle and the muscle exposed to either CN- or to PO2 less than 1.5 mmHg up to development of maximal Fu (Fumax) was similar at 1- and 100-Hz perturbations. Less profound hypoxia (PO2 6-10 mmHg) resulted in spontaneous sarcomere activity during the rise in Fu, and an increase in the ratio of stiffness at 100 Hz to stiffness at 1 Hz was detected. When oxidative phosphorylation was inhibited by CN- (2 mM) while the muscle was stimulated in the absence of both Ca2+ and Na+ (choline+substituted), the addition of Na+ at the time at which Fu had reached 30-40% of Fumax did not affect the rate of rise of Fu. These results show that the development of Fu during more complete anoxia in rat trabeculae is completely due to the formation of rigor links and that Ca2(+)-dependent cross-bridge activation can contribute to the rise in Fu during less severe hypoxia.

scholarly journals Reduced contraction strength with increased intracellular [Ca 2+ ] in left ventricular trabeculae from failing rat hearts

2003 ◽  
Vol 546 (2) ◽  
pp. 537-550 ◽  
Author(s):  
Marie‐Louise Ward ◽  
Adèle J. Pope ◽  
Denis S. Loiselle ◽  
Mark B. Cannell
Keyword(s):  
Left Ventricular ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Ventricular Trabeculae

scholarly journals Regional increase in extracellular potassium can be arrhythmogenic due to nonuniform muscle contraction in rat ventricular muscle

2012 ◽  
Vol 302 (11) ◽  
pp. H2301-H2309 ◽  
Author(s):  
Masahito Miura ◽  
Taiki Hattori ◽  
Naomi Murai ◽  
Tsuyoshi Nagano ◽  
Taichi Nishio ◽  
...  
Keyword(s):  
Sarcomere Length ◽  
Extracellular Potassium ◽  
Ventricular Muscle ◽  
Contraction Coupling ◽  
Exposed Region ◽  
Intracellular Ca ◽  
Restricted Region ◽  
Butanedione Monoxime ◽  
Global Increase ◽  
Ventricular Trabeculae

In the ischemic myocardium, extracellular potassium ([K+]o) increases to ≥20 mmol/l. To determine how lethal arrhythmias occur during ischemia, we investigated whether the increased spatial pattern of [K+]o, i.e., a regional or a global increase, affects the incidence of arrhythmias. Force, sarcomere length, membrane potential, and nonuniform intracellular Ca2+ ([Ca2+]i) were measured in rat ventricular trabeculae. A “regional” or “global” increase in [K+]o was produced by exposing a restricted region of muscle to a jet of 30 mmol/l KCl or by superfusing trabeculae with a solution containing 30 mmol/l KCl, respectively. The increase in [Ca2+]i (CaCW) during Ca2+ waves was measured (24°C, 3.0 mmol/l [Ca2+]o). A regional increase in [K+]o caused nonuniform [Ca2+]i and contraction. In the presence of isoproterenol, the regional increase in [K+]o induced sustained arrhythmias in 10 of 14 trabeculae, whereas the global increase did not induce such arrhythmias. During sustained arrhythmias, Ca2+ surged within the jet-exposed region. In the absence of isoproterenol, the regional increase in [K+]o increased CaCW, whereas the global increase decreased it. This increase in CaCW with the regional increase in [K+]o was not suppressed by 100 μmol/l streptomycin, whereas it was suppressed by 1) a combination of 10 μmol/l cilnidipine and 3 μmol/l SEA0400; 2) 20 mmol/l 2,3-butanedione monoxime; and 3) 10 μmol/l blebbistatin. A regional but not a global increase in [K+]o induces sustained arrhythmias, probably due to nonuniform excitation-contraction coupling. The same mechanism may underlie arrhythmias during ischemia.

Strain softening is not present during axial extensions of rat intact right ventricular trabeculae in the presence or absence of 2,3-butanedione monoxime

2004 ◽  
Vol 286 (2) ◽  
pp. H708-H715 ◽  
Author(s):  
R. S. Kirton ◽  
A. J. Taberner ◽  
A. A. Young ◽  
P. M. F. Nielsen ◽  
D. S. Loiselle
Keyword(s):  
Right Ventricular ◽  
Strain Softening ◽  
Muscle Length ◽  
Random Order ◽  
Left Ventricular ◽  
Softening Behavior ◽  
Rat Hearts ◽  
Butanedione Monoxime ◽  
Muscle Compliance ◽  
Ventricular Trabeculae

Recent studies of passive myocardial mechanics have shown that strain softening behavior is present during both inflation of isolated whole rat hearts and shearing of tissue blocks taken from the left ventricular free wall in pigs. Strain softening is typically manifested by a stiffer forceextension relation in the first deformation cycle relative to subsequent cycles and is distinguished from viscoelasticity by a lack of recovery of stiffness, even after several hours of rest. The causes of this behaviour are unknown. We investigated whether strain softening is observed in uniaxial extensions of intact, viable, rat right ventricular (RV) cardiac trabeculae. Stretch and release cycles of 5%, 10%, and 15% muscle length were applied at a constant velocity at 26°C. Muscles were tested in random order in the presence and absence of 50 mM 2,3-butanedione monoxime (BDM). Whereas strain softening was displayed by nonviable trabeculae, it was not observed in viable preparations undergoing physiologically relevant extensions whether in the presence or absence of BDM. BDM also had no effect on passive compliance. There was a reversible increase of muscle compliance between the first and subsequent cycles, with recovery after 30 s of rest, independent of the presence of BDM. We conclude that strain softening is neither intrinsic to viable rat RV trabeculae nor influenced by BDM and that passive trabeculae compliance is not altered by the addition of BDM.

Sarcomere relaxation in hamster diaphragm muscle

1996 ◽  
Vol 81 (2) ◽  
pp. 858-865 ◽  
Author(s):  
C. Coirault ◽  
D. Chemla ◽  
I. Suard ◽  
J. C. Pourny ◽  
Y. Lecarpentier
Keyword(s):  
Sarcomere Length ◽  
Peak Velocity ◽  
Muscle Tension ◽  
Muscle Length ◽  
Laser Diffraction ◽  
Diaphragm Muscle ◽  
Second Phase ◽  
Maximum Extent ◽  
Sarcomere Relaxation

We characterized instantaneous sarcomere relaxation over the load continuum in isolated hamster diaphragm muscles by means of laser diffraction. In afterloaded twitches, sarcomere relaxation displayed two consecutive phases. The bulk of sarcomere lengthening occurred during the first phase and corresponded in time to muscle lengthening. The second phase of sarcomere relaxation was slower and corresponded in time to tension decay. At initial muscle length, the peak velocity of sarcomere lengthening (SVL) was linearly related to both the maximum extent of sarcomere shortening (delta SL) and sarcomere length at peak shortening (SLmin; each P < 0.01). Varying preload modified the SVL vs. SLmin relationship but not the SVL vs. delta SL relationship. At a given preload, muscle tension decay began at a similar sarcomere length, regardless of the afterload level. In conclusion, our results support the role played by sarcomere length in regulating the diaphragm muscle-lengthening rate but not the rate of tension decline.

Morphological Basis of the Disparity Between Muscle Length and Sarcomere Length in the Myocardium

1973 ◽  
Vol 31 ◽  
pp. 422-423
Author(s):  
G.E. Adomian ◽  
L. Chuck ◽  
W.W. Pannley
Keyword(s):  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Muscle Length ◽  
Contractile Force ◽  
Direct Function ◽  
Morphological Basis ◽  
Tension Curve

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.

(-)-Terpinen-4-ol changes intracellular Ca 2+ handling and induces pacing disturbance in rat hearts

2017 ◽  
Vol 807 ◽  
pp. 56-63 ◽  
Author(s):  
Antonio Nei Santana Gondim ◽  
Aline Lara ◽  
Artur Santos-Miranda ◽  
Danilo Roman-Campos ◽  
Sandra Lauton-Santos ◽  
...  
Keyword(s):  
Rat Hearts ◽  
Intracellular Ca

scholarly journals Attenuation of extracellular ATP response in cardiomyocytes isolated from hearts subjected to ischemia-reperfusion

2005 ◽  
Vol 289 (2) ◽  
pp. H614-H623 ◽  
Author(s):  
Harjot K. Saini ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Cardiac Function ◽  
Positive Inotropic Effect ◽  
Ischemia Reperfusion ◽  
Cardiac Contractility ◽  
Extracellular Atp ◽  
Binding Characteristics ◽  
Rat Hearts ◽  
The Status ◽  
Intracellular Ca ◽  
Isolated Rat

Extracellular ATP is known to augment cardiac contractility by increasing intracellular Ca2+ concentration ([Ca2+]i) in cardiomyocytes; however, the status of ATP-mediated Ca2+ mobilization in hearts undergoing ischemia-reperfusion (I/R) has not been examined previously. In this study, therefore, isolated rat hearts were subjected to 10–30 min of global ischemia and 30 min of reperfusion, and the effect of extracellular ATP on [Ca2+]i was measured in purified cardiomyocytes by fura-2 microfluorometry. Reperfusion for 30 min of 20-min ischemic hearts, unlike 10-min ischemic hearts, revealed a partial depression in cardiac function and ATP-induced increase in [Ca2+]i; no changes in basal [Ca2+]i were evident in 10- or 20-min I/R preparations. On the other hand, reperfusion of 30-min ischemic hearts for 5, 15, or 30 min showed a marked depression in both cardiac function and ATP-induced increase in [Ca2+]i and a dramatic increase in basal [Ca2+]i. The positive inotropic effect of extracellular ATP was attenuated, and the maximal binding characteristics of 35S-labeled adenosine 5′-[γ-thio]triphosphate with crude membranes from hearts undergoing I/R was decreased. ATP-induced increase in [Ca2+]i in cardiomyocytes was depressed by verapamil and Cibacron Blue in both control and I/R hearts; however, this response in I/R hearts, unlike control hearts, was not affected by ryanodine. I/R-induced alterations in cardiac function and ATP-induced increase in [Ca2+]i were attenuated by treatment with an antioxidant mixture and by ischemic preconditioning. The observed changes due to I/R were simulated in hearts perfused with H2O2. The results suggest an impairment of extracellular ATP-induced Ca2+ mobilization in I/R hearts, and this defect appears to be mediated through oxidative stress.

Abstract 5402: Two Photon Microscopy Measurements Of Sub-epicardial Sarcomere Length In Perfused Rat Hearts

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Patrizia Camelliti ◽  
Gil Bub ◽  
Daniel J Stuckey ◽  
Christian Bollensdorff ◽  
Damian J Tyler ◽  
...  
Keyword(s):  
Sarcomere Length ◽  
Left Ventricular ◽  
Model Systems ◽  
Future Research ◽  
Fundamental Parameter ◽  
Rat Hearts ◽  
Perfused Hearts ◽  
Over Time

Sarcomere length (SL) is a fundamental parameter underlying the Frank Starling relation in the heart, as it offers an absolute representation of myocardial stretch. Previous studies addressed the Frank Starling relation by measuring SL in isolated myocytes or muscle strips. Here, we report first data obtained using a novel technique to measure sub-epicardial SL in perfused hearts. Rat hearts were Langendorff perfused (normal Tyrode solution) at a constant pressure of 90mmHg, labeled with the fluorescent membrane marker di-4-ANEPPS, and then arrested with high-K + Tyrode for either 2-photon microscopy (n=4) or MRI (n=4). Image analysis software was developed to extract SL at the cell level from >1,400 2-photon images (Fig 1 ) and correct for cell angle. SL increased by 10±2 % between 30 and 80 min of perfusion (1.98±0.04 to 2.17±0.03 μm; p<0.05; Fig 1 ). Measurements of left ventricular myocardial volume (LVMV) were made in vivo and in perfused hearts using 3D MRI. LVMV increased by 24±7% from in vivo to 30 min of perfusion, and by 11±3 % between 30 and 90 min (539±35; 664±44; 737±49 mm 3 , respectively; p<0.05; Fig 1 ). We show that SL can be measured in isolated perfused hearts. The method allowed monitoring of changes in SL over time, and showed that SL and LVMV increase to a similar extent during 30–80 min perfusion with crystalloid solution, probably due to tissue oedema. This result, together with the increase in LVMV during the first 30 min, highlights the pronounced differences between in vivo , in situ , and in vitro model systems for studies of cardiac physiology and mechanics. Future research will compare changes in SL in healthy hearts and disease models involving contractile dysfunction. Figure 1: Left: 2-photon microscopy image of di-4-ANEPPS labeled myocardium. Right: SL and LVMV changes over time.

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