The relation of age to the duration of contraction, ejection, and relaxation of the normal human heart

Harrison, Tinsley R.; Dixon, Kelly S.; Russell, Richard O.; Bidwai, P. S.; Coleman, Henry Neal

doi:10.1016/0002-8703(64)90370-9

Cited by 126 publications

(33 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…At the same time, the rise of the sys temic blood pressure and total peripheral vascular resistance and reduction of the heart rate were revealed in old cats and dogs only. It should be noted that such a trend in age-related changes was described earlier in man as well [Harrison et al, 1964;Korkushko, 1983;Fleg, 1986], Table II shows that IH and IPM of old rats exhibited the tendency to the reduction of the peak rate of tension fall only; the parameters characterizing contraction re mained at the same level as in adult ani mals.…”

Section: Resultssupporting

confidence: 66%

Contractile Function and Ca<sup>2+</sup> Transport System of Myocardium in Ageing

et al. 1988

View full text Add to dashboard Cite

Experiments with animals with various species-specific life span (rats, rabbits, cats, dogs) and different models (in situ heart, isolated perfused heart, isolated papillary muscle) have proved the reduction of functional capacity of the ageing heart. Diversely directional age-dependent shifts have been established involving myocardial Ca²⁺ transport system, i.e. an increase in the rate of Na⁺-Ca²⁺ exchange and passive Ca²⁺ transport across sarcolemma and a decrease in its Ca²⁺-binding capacity and a decrease in Ca²⁺ accumulation by sarcoplasmic reticulum and mitochondria (Ca²⁺ uptake). The experiments revealed a decrease in the Ca²⁺ ATPase myosin activity in the myocardium of aged animals and absence of age changes in the K⁺ ATPase activity. The findings obtained suggest that the development in the cardiac contractile function disorders in ageing largely depends on the age-related changes in the Ca²⁺ transport system.

show abstract

Section: Resultssupporting

confidence: 66%

Contractile Function and Ca<sup>2+</sup> Transport System of Myocardium in Ageing

et al. 1988

View full text Add to dashboard Cite

show abstract

“…First, because μtissues on stiff substrates generated more force to attain similar magnitudes of work as on moderate substrates, energy demands in stiff microenvironments are likely greater, which could contribute to metabolic remodeling that accompanies cardiomyopathies such as pathological hypertrophy (54). Second, contraction cycle duration increased on stiff substrates, similar to observations in aging myocardium (45,46), suggesting that decreased tissue compliance is sufficient to disrupt contraction cycle dynamics and could contribute to altered force-frequency relationships (47). Finally, the average peak systolic longitudinal tension generated by μtissues was uncorrelated to tissue geometry only on stiff substrates, suggesting that structural remodeling of myocyte shape, which is an important compensatory mechanism, is adaptive only in cellular microenvironments with mechanical compliances corresponding to the healthy heart.…”

Section: Discussionmentioning

confidence: 80%

“…Previous reports observed that contraction cycle duration is prolonged in aging myocardium (45,46) and that force-frequency relationships are defective in heart failure models (47). We asked if microenvironmental elasticity regulates contraction cycle dynamics.…”

mentioning

confidence: 95%

Cooperative coupling of cell-matrix and cell–cell adhesions in cardiac muscle

McCain

Lee

Aratyn-Schaus

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

159

162

View full text Add to dashboard Cite

Adhesion between cardiac myocytes is essential for the heart to function as an electromechanical syncytium. Although cell-matrix and cell-cell adhesions reorganize during development and disease, the hierarchical cooperation between these subcellular structures is poorly understood. We reasoned that, during cardiac development, focal adhesions mechanically stabilize cells and tissues during myofibrillogenesis and intercalated disc assembly. As the intercalated disc matures, we postulated that focal adhesions disassemble as systolic stresses are transmitted intercellularly. Finally, we hypothesized that pathological remodeling of cardiac microenvironments induces excessive mechanical loading of intercalated discs, leading to assembly of stabilizing focal adhesions adjacent to the junction. To test our model, we engineered μtissues composed of two ventricular myocytes on deformable substrates of tunable elasticity to measure the dynamic organization and functional remodeling of myofibrils, focal adhesions, and intercalated discs as cooperative ensembles. Maturing μtissues increased systolic force while simultaneously developing into an electromechanical syncytium by disassembling focal adhesions at the cell-cell interface and forming mature intercalated discs that transmitted the systolic load. We found that engineering the microenvironment to mimic fibrosis resulted in focal adhesion formation adjacent to the cell-cell interface, suggesting that the intercalated disc required mechanical reinforcement. In these pathological microenvironments, μtissues exhibited further evidence of maladaptive remodeling, including lower work efficiency, longer contraction cycle duration, and weakened relationships between cytoskeletal organization and force generation. These results suggest that the cooperative balance between cell-matrix and cell-cell adhesions in the heart is guided by an architectural and functional hierarchy established during development and disrupted during disease.adherens junctions | sarcomere | mechanotransduction | extracellular matrix I n the adult heart, healthy ventricular tissue is characterized by spatial segregation of cell-matrix adhesions to transverse myocyte borders (1) and cell-cell adhesions to longitudinal myocyte borders (2). Many cardiomyopathies are characterized by lateralization of cell-cell adhesions (3-5), increased expression of cell-matrix adhesions (6, 7), and arrhythmogenesis (8), suggesting that spatially organized adhesion is essential for effective eletromechanical coupling (9). Although in vivo studies have shown that localization of cell-matrix and cell-cell adhesions is developmentally regulated (10-13), the factors that regulate their assembly and disassembly are not well understood.Cell-matrix adhesions are especially important during organogenesis, anchoring developing cells and tissues to the extracellular matrix (ECM) (14) and directing cell migration (15-17). As development progresses, cell-matrix adhesions must selectively disassemble so that cell-cell adhesions can f...

show abstract

“…In subjects in the resting supine position, a small, but significant, in crease of LVET with age has been found by others [19,61]. These in vestigators based their conclusion on the fact that the regression coef ficients of LVET on HR for young and old subjects were statistically different.…”

Section: V E T Intervalmentioning

confidence: 80%

Systolic Time Intervals at Rest and during Exercise

Cardús¹,

Vera²

1974

Cardiology

View full text Add to dashboard Cite

Measurements of the electromechanical systole (QS₂) and its components: electromechanical delay (QS₁), isovolumic contraction time (ICT), and left ventricular ejection time (LVET), were conducted on 30 healthy men at rest and during exercise of varying intensity. The measurements were performed through simultaneous, non-invasive recordings of the electrocardiogram, phonocardiogram, and carotidogram. The conclusions are: (1) QS₂ and its components are principally correlated to the duration of the cardiac cycle (RR); (2) in changing posture from supine to sitting, the mean QS_t and mean ICT tend to increase, but these changes are not statistically significant. LVET and QS₂ are both significantly shortened; (3) during exercise there is a decrease in the mean values of QS_1’ ICT, LVET, and QS₂. The degree of LVET shortening is not as great as predicted by the ‘resting’ regression equation; (4) variations in arterial blood pressure and work load do not significantly affect systolic time intervals; (5) the effect of age on systolic time intervals is difficult to assess and needs further investigation.

show abstract

The relation of age to the duration of contraction, ejection, and relaxation of the normal human heart

Cited by 126 publications

References 12 publications

Contractile Function and Ca<sup>2+</sup> Transport System of Myocardium in Ageing

Contractile Function and Ca<sup>2+</sup> Transport System of Myocardium in Ageing

Cooperative coupling of cell-matrix and cell–cell adhesions in cardiac muscle

Systolic Time Intervals at Rest and during Exercise

Contact Info

Product

Resources

About