scholarly journals Do right-ventricular trabeculae gain energetic advantage from having a greater velocity of shortening?

2017 ◽  
Vol 595 (20) ◽  
pp. 6477-6488 ◽  
Author(s):  
Toan Pham ◽  
June-Chiew Han ◽  
Andrew Taberner ◽  
Denis Loiselle
Keyword(s):  
Right Ventricular ◽  
Velocity Of Shortening ◽  
Ventricular Trabeculae

scholarly journals Fractal Analysis of Right Ventricular Trabeculae in Pulmonary Hypertension

Radiology ◽  
2018 ◽  
Vol 288 (2) ◽  
pp. 386-395 ◽  
Author(s):  
Timothy J. W. Dawes ◽  
Jiashen Cai ◽  
Marina Quinlan ◽  
Antonio de Marvao ◽  
Philip J. Ostrowski ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Fractal Analysis ◽  
Ventricular Trabeculae

Unloaded shortening velocity of skinned rat myocardium: effects of volatile anesthetics

1990 ◽  
Vol 259 (4) ◽  
pp. H1118-H1125 ◽  
Author(s):  
J. S. Herland ◽  
F. J. Julian ◽  
D. G. Stephenson
Keyword(s):  
Isometric Force ◽  
Dose Dependence ◽  
Test Method ◽  
Dose Response Relationship ◽  
Shortening Velocity ◽  
Velocity Of Shortening ◽  
Cross Bridges ◽  
Dose Levels ◽  
Ventricular Trabeculae ◽  
Unloaded Velocity

The slack test method has been adapted for measurement of unloaded velocity of shortening in rat ventricular trabeculae that were skinned with saponin (50 micrograms/ml for 30 min). The method was sensitive enough to detect a 17% reversible change in the unloaded velocity of shortening produced by a 3 degrees C change in temperature. At pCa 5.30 (80-90% activation), halothane, enflurane, and isoflurane each slowed the shortening velocity by 25-30% at dose levels of 8 mM or greater but not at 4 mM or less. At pCa 5.48 (50-60% activation), halothane slowed the shortening velocity by 20-45% at dose levels of 4 mM or greater but not at 2 mM. The slowing effect of anesthetics on shortening velocity showed saturation at 8 mM for halothane, enflurane, and isoflurane when activation was at pCa 5.30. Saturation occurred at 4 mM for halothane when the pCa was 5.48. This result indicates that the dose-response relationship may be narrow, such that it can be demonstrated between 2 and 4 mM halothane for pCa 5.48 and between 4 and 8 mM halothane for pCa 5.30. The anesthetic dose dependence of isometric force and length axis intercept did not generally follow the same relationship as for the shortening velocity. Thus in several instances force did not significantly decrease when the velocity of shortening did. This may be interpreted as lack of simple inhibition by anesthetics on the number of interacting cross-bridges and as direct influence by anesthetics on the cross-bridge cycle.

Spontaneous mechanical alternans in papillary muscles from atherosclerotic rabbits

1980 ◽  
Vol 239 (5) ◽  
pp. H674-H680
Author(s):  
D. W. Peterson ◽  
C. A. Napolitano ◽  
D. W. Griffith
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Right Ventricular ◽  
Lipid Composition ◽  
Maximum Rate ◽  
Maximum Velocity ◽  
Atherogenic Diet ◽  
Papillary Muscles ◽  
Velocity Of Shortening ◽  
Induced Changes ◽  
Develop Tension

Mechanical alternans developed spontaneously in 5 of 17 right ventricular papillary muscles from atherosclerotic rabbits. The rabbits had eaten an atherogenic diet of 5% lard, 5% peanut oil, 0.5% cholesterol, and 89.5% rabbit pellets for 116-184 days. In one muscle mechanical alternans developed slowly and persisted. When the condition had developed fully, in the weaker contraction the muscle shortened only 20% as far when contracting isotonically and developed only 38% as much tension when contracting isometrically. Added to the superfusate, calcium (5.0 mM) or norepinephrine (1.5 X 10(-5) M) abolished the alternans. In four muscles mechanical alternans was only temporary. Compared with the 12 muscles that did not develop alternans, these 4, when contracting isometrically 12 times/min but not in alternans, had longer latency and required more time to develop tension at the maximum rate and to develop peak tension. Contracting isotonically, they required more time to accelerate to maximum velocity of shortening and to shorten maximally. Raising the contraction frequency to 24/min decreased the differences in performance between the two groups. Norepinephrine (1.5 X 10(-5) M) made the differences smaller still. We think that both the mechanical alternans and the differences in performance between the muscles that developed alteranans and those that did not resulted from a defect in the cardiac cell's handling of calcium. Diet-induced changes in the lipid composition of the sarcoplasmic reticulum or sarcolemma or both seem probable causes.

scholarly journals Strain softening behaviour in nonviable rat right-ventricular trabeculae, in the presence and the absence of butanedione monoxime

2004 ◽  
Vol 89 (5) ◽  
pp. 593-604 ◽  
Author(s):  
R. S. Kirton ◽  
A. J. Taberner ◽  
P. M. F. Nielsen ◽  
A. A. Young ◽  
D. S. Loiselle
Keyword(s):  
Right Ventricular ◽  
Strain Softening ◽  
Softening Behaviour ◽  
Butanedione Monoxime ◽  
Ventricular Trabeculae

scholarly journals Magnitude of length-dependent changes in contractile properties varies with titin isoform in rat ventricles

2012 ◽  
Vol 302 (3) ◽  
pp. H697-H708 ◽  
Author(s):  
Jitandrakumar R. Patel ◽  
Jonathan M. Pleitner ◽  
Richard L. Moss ◽  
Marion L. Greaser
Keyword(s):  
Right Ventricular ◽  
Cardiac Muscle ◽  
Differential Expression ◽  
Sarcomere Length ◽  
Passive Force ◽  
Wild Type ◽  
Titin Isoforms ◽  
Rat Ventricle ◽  
Mutant Homozygote ◽  
Ventricular Trabeculae

The effects of differential expression of titin isoforms on sarcomere length (SL)-dependent changes in passive force, maximum Ca2+-activated force, apparent cooperativity in activation of force ( nH), Ca2+ sensitivity of force (pCa50), and rate of force redevelopment ( ktr) were investigated in rat cardiac muscle. Skinned right ventricular trabeculae were isolated from wild-type (WT) and mutant homozygote (Ho) hearts expressing predominantly a smaller N2B isoform (2,970 kDa) and a giant N2BA-G isoform (3,830 kDa), respectively. Stretching WT and Ho trabeculae from SL 2.0 to 2.35 μm increased passive force, maximum Ca2+-activated force, and pCa50, and it decreased nH and ktr. Compared with WT trabeculae, the magnitude of SL-dependent changes in passive force, maximum Ca2+-activated force, pCa50, and nH was significantly smaller in Ho trabeculae. These results suggests that, at least in rat ventricle, the magnitude of SL-dependent changes in passive force, maximum Ca2+-activated force, pCa50, nH, and ktr is defined by the titin isoform.

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