Mechanics of Active Contraction in Cardiac Muscle: Part II—Cylindrical Models of the Systolic Left Ventricle

1993 ◽  
Vol 115 (1) ◽  
pp. 82-90 ◽  
Author(s):  
J. M. Guccione ◽  
L. K. Waldman ◽  
A. D. McCulloch
Keyword(s):  
Left Ventricle ◽  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Fiber Stress ◽  
Tension Development ◽  
Deactivation Model ◽  
Biomechanical Engineering ◽  
Asme Journal

Models of contracting ventricular myocardium were used to study the effects of different assumptions concerning active tension development on the distributions of stress and strain in the equatorial region of the intact left ventricle during systole. Three models of cardiac muscle contraction were incorporated in a cylindrical model for passive left ventricular mechanics developed previously [Guccione et al. ASME Journal of Biomechanical Engineering, Vol. 113, pp. 42-55 (1991)]. Systolic sarcomere length and fiber stresses predicted by a general “deactivation” model of cardiac contraction [Guccione and McCulloch, ASME Journal of Biomechanical Engineering, Vol. 115, pp. 72-81 (1993)] were compared with those computed using two less complex models of active fiber stress: In a time-varying “elastance” model, isometric tension development was computed from a function of peak intracellular calcium concentration, time after contraction onset and sarcomere length; a “Hill” model was formulated by scaling this isometric tension using the force-velocity relation derived from the deactivation model. For the same calcium ion concentration, the sarcomeres in the deactivation model shortened approximately 0.1 μm less throughout the wall at end-systole than those in the other models. Thus, muscle fibers in the intact ventricle are subjected to rapid length changes that cause deactivation during the ejection phase of a normal cardiac cycle. The deactivation model predicted rather uniform transmural profiles of fiber stress and cross-fiber stress distributions that were almost identical to those of the radial component. These three components were indistinguishable from the principal stresses. Transmural strain distributions predicted at end-systole by the deactivation model agreed closely with experimental measurements from the anterior free wall of the canine left ventricle.

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

1994 ◽  
Vol 266 (1) ◽  
pp. H68-H78 ◽  
Author(s):  
C. R. Cory ◽  
R. W. Grange ◽  
M. E. Houston
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Pressure Overload ◽  
Fold Increase ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Tension Development ◽  
Sequestration Potential

The loss of load-sensitive relaxation observed in the pressure-overloaded heart may reflect a strategy of slowed cytosolic Ca2+ uptake to yield a prolongation of the active state of the muscle and a decrease in cellular energy expenditure. A decrease in the potential of the sarcoplasmic reticulum (SR) to resequester cytosolic Ca2+ during diastole could contribute to this attenuated load sensitivity. To test this hypothesis, both in vitro mechanical function of anterior papillary muscles and the SR Ca2+ sequestration potential of female guinea pig left ventricle were compared in cardiac hypertrophy (Hyp) and sham-operated (Sham) groups. Twenty-one days of pressure overload induced by coarctation of the suprarenal, subdiaphragmatic aorta resulted in a 36% increase in left ventricular mass in the Hyp. Peak isometric tension, the rate of isometric tension development, and the maximal rates of isometric and isotonic relaxation were significantly reduced in Hyp. Load-sensitive relaxation were significantly reduced in Hyp. Load-sensitive relaxation quantified by the ratio of a rapid loading to unloading force step in isotonically contracting papillary muscle was reduced 50% in Hyp muscles. Maximum activity of SR Ca(2+)-adenosinetriphosphatase (ATPase) measured under optimal conditions (37 degrees C; saturating Ca2+) was unaltered, but at low free Ca2+ concentrations (0.65 microM), it was decreased by 43% of the Sham response. Bivariate regression analysis revealed a significant (r = 0.84; P = 0.009) relationship between the decrease in SR Ca(2+)-ATPase activity and the loss of load-sensitive relaxation after aortic coarctation. Stimulation of the SR Ca(2+)-ATPase by the catalytic subunit of adenosine 3',5'-cyclic monophosphate-dependent protein kinase resulted in a 2.6-fold increase for Sham but only a 1.6-fold increase for Hyp. Semiquantitative Western blot radioimmunoassays revealed that the changes in SR Ca(2+)-ATPase activity were not due to decreases in the content of the Ca(2+)-ATPase protein or phospholamban. Our data directly implicate a role for decreased SR function in attenuated load sensitivity. A purposeful downregulation of SR Ca2+ uptake likely results from a qualitative rather than a quantitative change in the ATPase and possibly one of its key regulators, phospholamban.

Myocardial mechanics predict hemodynamic performance during normal function and alcohol-induced dysfunction in rats

1991 ◽  
Vol 261 (6) ◽  
pp. H1880-H1888
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
P. Anversa
Keyword(s):  
Pressure Rise ◽  
Normal Function ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Papillary Muscles ◽  
Least Squares Regression ◽  
Tension Development ◽  
Myocardial Mechanics

To determine whether mechanical evaluation of muscle tissue removed from the myocardium can be employed as a direct indicator of cardiac contractile performance in situ, isometric and isotonic parameters of muscle mechanics in vitro were correlated with in vivo global functional characteristics of the same heart. Twelve-month-old animals maintained on standard food and water were employed as representative of normal cardiac function. Animals of identical age with left ventricular (LV) dysfunction induced by oral alcohol (30%) ingestion from 4 to 12 mo were utilized to represent depressed cardiac performance. Accordingly, 24 h after the establishment of the hemodynamic profile for a control or experimental heart, the LV posterior papillary muscle was removed from the same heart and examined isometrically and isotonically. Least squares regression analysis was employed to establish a correlation coefficient and P values between various in vitro and in vivo parameters. Hemodynamic measurements were performed under chloral hydrate anesthesia and LV pump performance was evaluated with respect to aortic and ventricular pressures and the rates of rise and decay of the LV pressure trace. Papillary muscles were evaluated with respect to timing parameters of the isometric and isotonic twitch, the first derivative of isometric tension development, and the speed of muscle shortening at increasing physiologic loads. LV peak rate of pressure rise and decay were then correlated with the various isometric and isotonic properties. Myocardial mechanics and hemodynamics revealed depressed function in the papillary muscles and hearts from alcoholic rats. Moreover, significant correlations were found between the LV rate of pressure change (peak +dP/dt and -dP/dt) and both isometric and isotonic twitch measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of estrogen on composition and function of cardiac muscle

1959 ◽  
Vol 196 (6) ◽  
pp. 1282-1285 ◽  
Author(s):  
T. M. King ◽  
W. V. Whitehorn ◽  
B. Reeves ◽  
R. Kubota
Keyword(s):  
Cardiac Muscle ◽  
Protein Concentration ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Albino Rats ◽  
Tension Development ◽  
Contractile System ◽  
General Action ◽  
And Function

In vitro tension development is significantly reduced in surviving left ventricular columnae carneae and ATP treated glycerol extracted fibers of ovariectomized albino rats. This reduction in contractility is paralleled by decrease in ventricular actomyosin content. Heart-body weight ratio, myocardial water content and total protein concentration are not abnormal. No changes in excitability or refractoriness of surviving bundles of castrate animals were found. Treatment with alpha estradiol, 0.1 µg/day, returned tension production and actomyosin concentration to the normal range. It is concluded that the contractile system of cardiac muscle, like that of the uterus, is dependent on estrogen. These data suggest a general action of the hormone on contractile protein synthesis in all types of muscle and have important implications regarding cardiac and other muscular functions.

Effects of hypoxia on cardiac growth in neonatal rat

1976 ◽  
Vol 231 (5) ◽  
pp. 1445-1450 ◽  
Author(s):  
M Hollenberg ◽  
N Honbo ◽  
AJ Samorodin
Keyword(s):  
Body Weight ◽  
Left Ventricle ◽  
Cardiac Muscle ◽  
Neonatal Period ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Low Oxygen ◽  
Cardiac Muscle Cells

To determine whether low oxygen environments enhance cardiac cell division in the neonatal period, newborn rat pups were reared for 21 days in 12-15% oxygen. Left ventricle and right ventricle weights were 30 and 180% greater than controls matched for body weight (P less than 0.001) as were left ventricle/body weight ratios (3.68+/-0.26 vs. 2.99+/-0.05 mg LV/g body wt,P less than 0.001). Left ventricular total DNA and DNA concentration was 95 and 48% greater than controls (P less than 0.001). Autoradiography confirmed that this increase in ventricular DNA resulted from an increased rate of division of cardiac muscle cells, fibroblast, and vascular endothelial cells. When [3H]thymidine was injected on day ), autoradiographs prepared on day 21 reflected an increased dilution of label in hypoxic rats consistent with enhanced proliferation. The labeling index and grains per nucleus of ventricular muscle cells was 25% (P less than 0.01) and 20% (P less than 0.02) less than controls, Thus, hypoxic stress applied early in the neonatal period augments the rate of division and ultimate number of cardiac muscle cells. Whether this enhancement results from a primary effect of oxygen or from secondary hemodynamic factors remains unknown.

Influence of poststimulation potentiation and heart rate on the fetal lamb heart

1975 ◽  
Vol 229 (2) ◽  
pp. 318-323 ◽  
Author(s):  
SE Kirkpatrick ◽  
J Naliboff ◽  
PT Pitlick ◽  
WF Friedman
Keyword(s):  
Heart Rate ◽  
Recovery Period ◽  
Control Level ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Atrial Pacing ◽  
Tension Development ◽  
Time To Peak ◽  
Fetal Lamb

Isolated cardiac muscle techniques and studies of the chronically instrumented fetal lamb heart were employed to evaluate the ability of fetal myocardium to exhibit poststimulation potentiation. Isometric tension development and the response to paired electrical stimulation were significantly reduced in isolated fetal ventricular myocardium when compared to the adult (P less than 0.001). As in the adult, increasing stimulation frequency raised fetal isometric tension via an increase in the rate of rise of tension development in the presence of reduction in time-to-peak tension. In seven fetal lambs the left ventricle was chronically instrumented with endocardial ultrasonic crystals and a high-fidelity micromanometer. After a 2-wk recovery period, heart rate was increased by atrial pacing from an average control level of 150 to 300 beats/min. Left ventricular dP/dt increased progressively and then fell beyond a heart rate of 270/min. When comparable pre- and immediate postpacing beats were analyzed, a step-wise increase in the velocity of left ventricular shortening and the mean rate of circumferential fiber shortening was observed in association with an increase in the extent of shortening. Thus, increases in the frequency of contraction exert a significant positive inotropic effect on the fetal heart.

RELATIONSHIP BETWEEN pH FALL AND INITIATION OF ISOTONIC CONTRACTION IN POSTMORTEM BEEF MUSCLE

1979 ◽  
Vol 59 (4) ◽  
pp. 639-647 ◽  
Author(s):  
R. W. CURRIE ◽  
F. H. WOLFE
Keyword(s):  
Cooling Rate ◽  
Sarcomere Length ◽  
Isometric Tension ◽  
Post Mortem ◽  
Tension Development ◽  
Isotonic Contraction ◽  
Light Load ◽  
Beef Muscles ◽  
Beef Muscle

Beef muscles were sampled at various times post-mortem both on and off carcass, and the pH, sarcomere length, and isotonic contraction profiles under various loads recorded. The results demonstrate that muscle under light load will begin to contract at pH 6.3 but more heavily loaded muscle will not contract until pH 5.8. Rapid pH fall produced an earlier initiation of contraction than slow pH fall, but the pH required for initiation of contraction under equal loads was the same. The results of isometric tension development followed by unrestrained contraction during the course of rigor development are presented. The authors suggest that both carcass cooling rate and rate of pH fall are implicated in prerigor contraction of postmortem beef muscle.

Effects of insulin on cardiac muscle contraction and responsiveness to norepinephrine

1976 ◽  
Vol 230 (5) ◽  
pp. 1360-1365 ◽  
Author(s):  
JC Lee ◽  
SE Downing
Keyword(s):  
Cardiac Muscle ◽  
Positive Inotropic Effect ◽  
Contractile Activity ◽  
Isometric Tension ◽  
Krebs Solution ◽  
Maximal Rate ◽  
Inotropic Action ◽  
Tension Development ◽  
Moderator Band ◽  
Negative Effect

The effects of insulin (In) on contractile activity of isolated cardiac muscle were studied in right ventricular moderator band (MB) of piglets and papillary muscle (PM) of cats and kittens. The muscles were bathed in modified Krebs solution containing 5.6 mM glucose at 30 degrees C and gassed with 95% O2 and 5% CO2. They were paced at 24 contractions per minute isometrically at Lmax. Addition of In (1 U/ml) to the bath induced a biphasic inotropic response to piglet MB. The initial negative effect was due to the preservative (0.2% phenol) in the regular commercial In solution. Following the transitory depression, both active isometric tension (AT) and maximal rate of tension development increased to a maximum (about 120% of control) within 15 min and then declined slightly toward control. Similar positive responses were observed in both cat and kitten PM, but without the initial negative effect. Maximal responses were not diminished by the absence of glucose in the bath. Increases in AT and dT/dt of both MB and PM in response to NE were significantly attenuated in the presence of In compared with untreated muscle. These findings demonstrate that In elicits a positive inotropic effect on mammalian cardiac muscle and that it impairs the inotropic action of NE.

Effects of pressure- or volume-overload hypertrophy on passive stiffness in isolated adult cardiac muscle cells

1996 ◽  
Vol 271 (6) ◽  
pp. H2575-H2583 ◽  
Author(s):  
S. Kato ◽  
M. Koide ◽  
G. Cooper ◽  
M. R. Zile
Keyword(s):  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Septal Defect ◽  
Myocardial Hypertrophy ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Passive Stiffness ◽  
Cardiac Muscle Cells ◽  
Adult Cats

It has been hypothesized that the changes in myocardial stiffness induced by chronic hemodynamic overloading are dependent on changes in the passive stiffness of the cardiac muscle cell (cardiocyte). However, no previous studies have examined the passive constitutive properties of cardiocytes isolated from animals with myocardial hypertrophy. Accordingly, changes in relative passive stiffness of cardiocytes isolated from animals with chronic pressure- or volume-overload hypertrophy were determined by examining the effects of anisosmotic stress on cardiocyte size. Anisosmotic stress was produced by altering superfusate osmolarity. Hypertrophied cardiocytes were enzymatically isolated from 16 adult cats with right ventricular (RV) pressure-overload hypertrophy induced by pulmonary artery banding (PAB) and from 6 adult cats with RV volume-overload hypertrophy induced by creating an atrial septal defect (ASD). Left ventricular (LV) cardiocytes from each cat served as nonhypertrophied, normally loaded, same-animal controls. Superfusate osmolarity was decreased from 305 +/- 3 to 135 +/- 5 mosM and increased to 645 +/- 4 mosM. During anisosmotic stress, there were no significant differences between hypertrophied RV and normal LV cardiocytes in pressure overload PAB cats with respect to percent change in cardiocyte area (47 +/- 2% in RV vs. 48 +/- 2% in LV), diameter (46 +/- 3% in RV vs. 48 +/- 2% in LV), or length (2.4 +/- 0.2% in RV vs. 2.0 +/- 0.3% in LV), or sarcomere length (1.5 +/- 0.1% in RV vs. 1.3 +/- 0.3% in LV). Likewise, there were no significant differences in cardiocyte strain between hypertrophied RV and normal LV cardiocytes from ASD cats. In conclusion, chronic pressure-overload hypertrophy and chronic volume-overload hypertrophy did not alter the cardiocyte response to anisosmotic stress. Thus chronic overload hypertrophy did not alter relative passive cardiocyte stiffness.

Anterior and posterior left ventricular sarcomere lengths behave similarly during ejection

1997 ◽  
Vol 272 (1) ◽  
pp. H469-H477 ◽  
Author(s):  
J. M. Guccione ◽  
W. G. O'Dell ◽  
A. D. McCulloch ◽  
W. C. Hunter
Keyword(s):  
Left Ventricle ◽  
Regional Differences ◽  
Sarcomere Length ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Regional Deformation ◽  
Absolute Measure ◽  
Radiopaque Markers ◽  
The Mean

Previous studies of regional differences in myocardial deformation between the anterior and posterior walls of the canine left ventricle were based on strain, which is not an absolute measure of deformation. We thus compared sarcomere lengths at anterior and posterior sites during ejection in isolated dog hearts. Cineradiographic imaging of regional deformation with radiopaque markers implanted near the midwall in five hearts and just below the epicardium in six hearts, combined with postmortem histology, allowed sarcomere length reconstruction throughout the cardiac cycle. The amount of sarcomere shortening accompanying left ventricular ejection was similar in both walls of the left ventricle for sarcomeres located at epicardial and midwall sites. The mean sarcomere length (taken at the middle of the ejecting range) was also similar between the anterior and posterior sites when averaged over all hearts. The similarity of sarcomere function held not only at end systole but throughout ejection and over wide ranges of ventricular pre- and afterloads. Hence functional measurements of relative myocardial shortening may not be indicative of regional sarcomere length heterogeneity.

Optimizing ventricular fibers: uniform strain or stress, but not ATP consumption, leads to high efficiency

2002 ◽  
Vol 283 (3) ◽  
pp. H1072-H1081 ◽  
Author(s):  
Marko Vendelin ◽  
Peter H. M. Bovendeerd ◽  
Jüri Engelbrecht ◽  
Theo Arts
Keyword(s):  
Ejection Fraction ◽  
Fiber Orientation ◽  
Sarcomere Length ◽  
High Efficiency ◽  
Element Model ◽  
Left Ventricular ◽  
Fiber Stress ◽  
Fiber Angle ◽  
Transverse Fiber ◽  
Bridge Model

The aim of this study was to investigate the influence of fiber orientation in the left ventricular (LV) wall on the ejection fraction, efficiency, and heterogeneity of the distributions of developed fiber stress, strain and ATP consumption. A finite element model of LV mechanics was used with active properties of the cardiac muscle described by the Huxley-type cross-bridge model. The computed variances of sarcomere length (SLvar), developed stress (DSvar), and ATP consumption (ATPvar) have several minima at different transmural courses of helix fiber angle. We identified only one region in the used design space with high ejection fraction, high efficiency of the LV and relatively small SLvar, DSvar, and ATPvar. This region corresponds to the physiological distribution of the helix fiber angle in the LV wall. Transmural fiber angle can be predicted by minimizing SLvar and DSvar, but not ATPvar. If ATPvarwas minimized, then the transverse fiber angle was considerably underestimated. The results suggest that ATP consumption distribution is not regulating the fiber orientation in the heart.

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