X-ray diffraction study of contracting heart muscle

Matsubara, Ichiro; Kamiyama, Asako; Suga, Hiroyuki

doi:10.1016/s0022-2836(77)80118-6

Cited by 24 publications

(27 citation statements)

References 14 publications

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“…The difference was statistically significant (P < 0.01). Both the systolic and the diastolic ratios were smaller than the ratio reported for the heart muscle not undergoing cyclic contractions (3.07), but were greater than the ratio reported for the heart muscle in rigor (0.37) (Matsubara, Kamiyama & Suga, 1977). …”

Section: Resultscontrasting

confidence: 68%

“…4 reveals that the mass of the material associated with the thin filaments increases as the state of the muscle shifted from one at the left (the quiescent state) towards the one at the right (rigor), and that this is accompanied by a decrease in the mass of the material associated with the thick filaments. Similar changes have been observed in skeletal muscle (Huxley, 1968;Haselgrove & Huxley, 1973) and heart muscle (Matsubara et al 1977), and have been attributed to the transfer of myosin projections from the vicinity of the thick filaments to that of the thin filaments. By making the crude assumption that the mass of the material transferred from the thick to the thin filaments as the heart muscle shifts from the quiescent to the rigor state (i.e.…”

Section: Fourier Projectionssupporting

confidence: 76%

“…This was indicated by the comparison between the cross-circulated and the hypodynamic prepara-318 X-RAY DIFFRACTION OF BEATING HEART tions. In the hypodynamic preparation, the myosin projections found in the vicinity of the thin filaments during the diastolic phase were 8-9 % of the total projections (Matsubara et al 1977). Since the diastolic tension of the cross-circulated preparation in which 51-52 % of the projections were found in the vicinity of the thin filaments during diastole did not differ significantly from that of the hypodynamic preparation, we conclude that most of these projections are not producing significant contractile force.…”

Section: Comparison With the Hypodynamic Preparationmentioning

confidence: 67%

“…not undergoing the cardiac cycle); B, diastolic state; C, systolic state; D, rigor. The density distributions for the diastolic and the systolic states were calculated from the intensities of the 1, 0 and the 1, 1 reflexions obtained in the present study, whereas the distributions for the quiescent and the rigor states were calculated from the data of Matsubara et al (1977). The larger peaks in each diagram represent the thick filaments and the smaller peaks represent the thin filaments.…”

Section: W~~~~~~~~~~~~~~~~~~~~~~ã -Ii_ Rfjr Jomentioning

confidence: 99%

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An X‐ray diffraction study of the cross‐circulated canine heart.

Matsubara¹,

Suga²,

Yagi³

1977

The Journal of Physiology

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SUMMARY1. The equatorial X-ray diffraction pattern was recorded from a papillary muscle of a cross-circulated canine heart at different phases of the cardiac cycle. The intensity ratio of the 1, 0 and the 1, 1 reflexions (II, dI, 1) was 0-79 in the systolic phase and 1-19 in the diastolic phase.2. Using the intensity ratio obtained, the approximate proportion of the myosin projections present in the vicinity of the thin filaments was calculated. This was 70-71 % in the systolic phase and 51-52 % in the diastolic phase of the total myosin projections.3. The peak systolic tension was roughly proportional to the proportion of the projections present in the vicinity of the thin filaments during systole.4. The projections which stayed in the vicinity of the thin filaments during diastole did not produce significant contractile force.

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Section: Resultscontrasting

confidence: 68%

Section: Fourier Projectionssupporting

confidence: 76%

Section: Comparison With the Hypodynamic Preparationmentioning

confidence: 67%

Section: W~~~~~~~~~~~~~~~~~~~~~~ã -Ii_ Rfjr Jomentioning

confidence: 99%

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An X‐ray diffraction study of the cross‐circulated canine heart.

Matsubara¹,

Suga²,

Yagi³

1977

The Journal of Physiology

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“…Moreover, we observed here that a small amount of myofilament lattice compression by application of 1% dextran (equivalent to 0.38 kPa applied osmotic compression) induced a change in the I 1,1 /I 1,0 intensity ratio from ϳ0.3 to ϳ0.45 in relaxed, isolated skinned myocardium. Various measurements of this parameter have been made previously in intact, nonskinned myocardium by Matsubara and colleagues (I 1,1 /I 1,0 ϭ 0.375) (23) and (I 1,1 /I 1,0 ϭ 0.581) (24), as well as Yagi and colleagues (I 1,1 /I 1,0 ϭ 0.4) (38) and (I 1,1 /I 1,0 ϭ 0.444) (37). Of interest, these values are similar to those observed in this present study in skinned rat cardiac trabeculae in the high-myofilament calcium sensitivity state, that is, those muscles that were compressed by application of Ͼ1.0% dextran (0.38 kPa).…”

Section: Discussionmentioning

confidence: 99%

Impact of osmotic compression on sarcomere structure and myofilament calcium sensitivity of isolated rat myocardium

Farman¹,

Walker²,

Tombe³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Farman, Gerrie P., John S. Walker, Pieter P. de Tombe, and Thomas C. Irving. Impact of osmotic compression on sarcomere structure and myofilament calcium sensitivity of isolated rat myocardium. Am J Physiol Heart Circ Physiol 291: H1847-H1855, 2006. First published June 2, 2006 doi:10.1152/ajpheart.01237.2005.-Changes in interfilament lattice spacing have been proposed as the mechanism underlying myofilament length-dependent activation. Much of the evidence to support this theory has come from experiments in which high-molecular-weight compounds, such as dextran, were used to osmotically shrink the myofilament lattice. However, whether interfilament spacing directly affects myofilament calcium sensitivity (EC50) has not been established. In this study, skinned isolated rat myocardium was osmotically compressed over a wide range (Dextran T500; 0 -6%), and EC50 was correlated to both interfilament spacing and I1,1/I1,0 intensity ratio. The latter two parameters were determined by X-ray diffraction in a separate group of skinned muscles. Osmotic compression induced a marked reduction in myofilament lattice spacing, concomitant with increases in both EC50 and I1,1/I1,0 intensity ratio. However, interfilament spacing was not well correlated with EC50 (r 2 ϭ 0.78). A much better and deterministic relationship was observed between EC50 and the I1,1/I1,0 intensity ratio (r 2 ϭ 0.99), albeit with a marked discontinuity at low levels of dextran compression; that is, a small amount of external osmotic compression (0.38 kPa, corresponding to 1% Dextran T500) produced a stepwise increase in the I1,1/I1,0 ratio concomitant with a stepwise decrease in EC50. These parameters then remained stable over a wide range of further applied osmotic compression (up to 6% dextran). These findings provide support for a "switch-like" activation mechanism within the cardiac sarcomere that is highly sensitive to changes in external osmotic pressure. skinned muscle; trabeculae; X-ray diffraction; dextran; osmotic pressure; myofilament length-dependent activation; regulation MYOFILAMENT LENGTH-DEPENDENT activation (LDA) is a phenomenon found in all striated muscle, but to varying extents, being a prominent feature of cardiac muscle (2,4,7,15,16) and the indirect flight muscle of insects (33) but is less prominent in skeletal muscle (17,26,32). LDA is defined as an increase in the amount of active force developed at longer sarcomere length for a given concentration of activating calcium ions. LDA is the underlying cellular mechanism that underlies the Frank-Starling law of the heart (16). This increase in myofilament calcium sensitivity is commonly measured by the EC 50 parameter, that is, the calcium concentration at which the active developed force is half that observed at a saturating calcium concentration. An understanding of the molecular mechanism(s) underlying LDA has remained elusive. A popular hypothetical mechanism for LDA is that changes in interfilament lattice spacing, usually estimated as changes in fiber width, are directly linke...

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Structure of Vertebrate Striated Muscle as Determined by X‐ray‐Diffraction Studies

Haselgrove

1983

Comprehensive Physiology

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The sections in this article are: Muscle Structure: An Overview Description of Low‐Angle Diffraction Patterns Interpretation of X‐Ray Patterns Theoretical Aspects Experimental Approaches Filament Lattice Lattice Spacing Filament Orientations Radial Electron‐Density Distribution Actin‐Containing Filaments Helix Parameters Thin‐Filament Regulation of Contraction Myosin‐Filament Backbone Axial Packing of Myosin Helical Packing of Myosin Axial Repeat of C Protein Cross Bridges Relaxed Muscle Rigor Muscle Contracting Muscle Analogues of ATP

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X-ray diffraction study of contracting heart muscle

Cited by 24 publications

References 14 publications

An X‐ray diffraction study of the cross‐circulated canine heart.

An X‐ray diffraction study of the cross‐circulated canine heart.

Impact of osmotic compression on sarcomere structure and myofilament calcium sensitivity of isolated rat myocardium

Structure of Vertebrate Striated Muscle as Determined by X‐ray‐Diffraction Studies

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