Some Quantitative Aspects of the Relation of Rhythm to the Contractile Force of Mammalian Ventricular Muscle

Garb, Solomon; Penna, Mario

doi:10.1152/ajplegacy.1955.182.3.601

Cited by 21 publications

(7 citation statements)

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“…However, the optimum prematurity interval always exceeds the minimum interval by a significant amount. This finding is in agreement with a previous study of the cat papillary muscle 21 and with results from atrial myocardium, 28 ' 29 but it conflicts with the generally held view. 11 " 14 The view that potentiation increases indefinitely with prematurity of the extra-activations may have arisen for several reasons: 1) determination of the minimum interval for potentiation by gradually decreasing the prematurity of the stimulus (see results, method II); 2) extrapolation from studies in which only single premature activations were used; 3) studies done at low temperatures which prolong the refractory period.…”

Section: Discussionsupporting

confidence: 88%

Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Koch‐Weser

1966

Circulation Research

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The strength of myocardial contraction is influenced directly and strongly by the intervals separating individual beats. The large number of studies on this phenomenon during the 95 years since its original recognition 1 have recently been reviewed. 2 Interval-dependent changes in the strength and time course of contraction result both from alterations in the duration of the active state and from changes in the degree of activation of the contractile element (shifts of the force-velocity curve). 2 Every activation of mammalian myocardium appears to leave behind two temporary changes in the muscle that have opposing effects on the degree of activation in subsequent beats. 2 ' 3 The extent of cumulation of both changes depends on rate and rhythm of contraction, and the interaction of their respective levels of cumulation can account for all interval-dependent variations in the degree of activation. 2 In ventricular heart muscle of most mammalian species the degree of activation and the rate of tension development in an isometric contraction increase steadily with frequency over the entire physiologic range. 2 ' 4 Deviation from regular rhythm changes contractile performance markedly even when the overall frequency of contraction remains constant. 2 Changes in contractile strength associated with premature beats were described 80 years ago 5 and have since been studied extensively. 2 ' 6 In mammalian ventricular muscle a premature contraction is weaker than the preceding beats. Following a premature beat several regular contractions are increased in strength, and this potentiation cumulates if the premature activations are continually repeated. 7 " 1 " If every other activation of heart muscle is a very premature one, the mechanical result of these becomes negligible while contractility in the regular beats is greatly potentiated. Because of its possible clinical applications such sustained potentiation has recently attracted much attention. 11 " 18 Despite this renewed interest many questions concerning potentiation by premature activations remain unsettled. Among these are 1) the relationship between premature stimulus, propagated action potential, mechanical event and the potentiation of the regular beat; 2) the influence of the basal frequency of contraction and of the degree of prematurity on the extent of potentiation; 3) the question whether summation of contractions or increased release of endogenous norepinephrine play any role in potentiation by premature activations; and 4) the effect of premature activations on the resting length-tension relationship. During the past two years we have investigated these questions using isolated papillary muscles of young kittens, a tissue which is representative of the ventricular myocardium of most mammalian species including man. 2

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Section: Discussionsupporting

confidence: 88%

Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Koch‐Weser

1966

Circulation Research

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“…The possibility that some other parameter which is the true determinant of ventricular contraction always correlates closely with LVEDSL or LVEDP cannot be excluded from these studies, nor from any of the classic observations which have led to the view that the length and tension existing in a muscle at the onset of contraction are important determinants of the character of the contraction (30)(31)(32)(33). It is unlikely that the duration of the preceding diastole, per se, is the determinant of the characteristics of the subsequent ventricular contraction, since experiments performed on isolated cardiac muscle preparations indicate that the force of muscular contraction actually varies inversely with the duration of diastole (34,35).…”

Section: Discussionmentioning

confidence: 99%

Studies on Starling's Law of the Heart. Iii. Observations in Patients With Mitral Stenosis and Atrial Fibrillation on the Relationships Between Left Ventricular End-Diastolic Segment Length, Filling Pressure, and the Characteristics of Ventricular Contraction *

Braunwald¹,

Frye²,

Aygen³

et al. 1960

J. Clin. Invest.

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Although 45 years have now elapsed since Starling's Linacre lecture on the "Law of the Heart Beat" (1), considerable controversy is still centered around the question of the applicability of this fundamental principle to the human heart. In several investigations the Starling concept has been examined by attempts to reproduce in man those experiments on the Starling heart-lung preparation in which its responses to acute changes in venous return were studied (2-6). In most of these investigations no consistent relationship between the filling pressure on the right side of the heart and the cardiac output was apparent. In experiments on the intact dog (7), Rushmer, Smith and Franklin have shown that the augmentation of cardiac work which accompanies muscular exercise is not associated with an increase in left ventricular dimensions. These experiments, when taken together with the observations on man (2-6), have cast considerable doubt on the hypothesis that the Frank-Starling mechanism is involved in the regulation of cardiac performance.In the present investigation, portions of which have been presented in preliminary form elsewhere (8) to make such observations with the heart functioning with a relatively constant level of circulating catecholamines and of sympathetic stimulation, in view of the importance of these factors on myocardial performance (9).When the inflow of blood into the left ventricle is not impeded, most of the filling of this chamber occurs during the first portion of diastole, i.e., during the so-called rapid filling phase (10). When the heart rate is slow, this phase of the cardiac cycle is not encroached upon, diastasis is present (11,12), and changes in the duration of diastole do not profoundly modify ventricular filling. In patients with mitral stenosis, the obstruction to left atrial emptying prevents the left ventricle from filling rapidly during early diastole (12). Accordingly, it might be anticipated that in patients with mitral stenosis, and irregular ventricular rates due to atrial fibrillation, at any given left atrial pressure, beat-to-beat variations in the filling of the left ventricle take place due to alterations in the duration of the filling period. It was considered that if Starling's law of the heart operated in patients with mitral stenosis, the characteristics of each left ventricular contraction should appear to be a function of the previous end-diastolic fiber length or end-diastolic pressure, i.e., beats evidencing a relatively great force of ventricular contraction should be preceded by greater enddiastolic fiber lengths and filling pressures than beats evidencing a relatively smaller force of ventricular contraction. On the other hand, if Starling's law did not operate in these patients, then no clear relationship should be evident between ventricular end-diastolic fiber length or end-diastolic pressure and the characteristics of the subsequent contraction. 1874

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“…1) is ccjmparable in rat trabecula (cf. Schouten et al 1987 dium (Hoffman et al 1956), cat heart (Garb and Penna 1956), rabbit papillany nauscles (Anderson et al 19'73), and human myocardium (Quaegebeur ct al. 198'7).…”

Section: Ivili-~la"mentioning

confidence: 99%

Excitation–contraction coupling in myocardium: implications of calcium release and Na⁺–Ca²⁺ exchange

Keurs¹,

Schouten²,

Bucx³

et al. 1987

Can. J. Physiol. Pharmacol.

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In this paper, we present evidence in support of the hypothesis that electrogenic Na+-Ca2+ exchange is responsible for three phenomena in rat cardiac muscle: the slow repolarization phase of the action potential, the time course of the mechanical recovery process, and the development of triggered arrhythmias. It was shown that the duration of the slow phase of repolarization of the action potential varies in proportion to the Na+ concentration gradient and inversely with the Ca2+ concentration gradient over the cell membrane. This suggested that Na+-Ca2+ exchange can generate a current of sufficient magnitude to maintain the membrane depolarized at a level of -60 mV. The mechanical restitution process of rat cardiac trabeculae was shown to exhibit three phase. The first phase, alpha, probably reflects rapid transport of calcium in the sarcoplasmic reticulum from the uptake sites to the release sites. After the initial increase of force during alpha, force rises further during phase beta and then declines during phase gamma. During all phases, force increases with the extracellular calcium concentration. beta is accelerated by preceding extrasystoles, while an increase of the heart rate causes force to increase at approximately the same rate but to a higher level during phase beta. These observations are compatible with a model in which the sarcoplasmic reticulum sequesters calcium from the cytosol, while the membrane of the sarcoplasmic reticulum is assumed to exhibit also a small leak of calcium into the cytosol.(ABSTRACT TRUNCATED AT 250 WORDS)

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Some Quantitative Aspects of the Relation of Rhythm to the Contractile Force of Mammalian Ventricular Muscle

Cited by 21 publications

References 0 publications

Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Studies on Starling's Law of the Heart. Iii. Observations in Patients With Mitral Stenosis and Atrial Fibrillation on the Relationships Between Left Ventricular End-Diastolic Segment Length, Filling Pressure, and the Characteristics of Ventricular Contraction *

Excitation–contraction coupling in myocardium: implications of calcium release and Na⁺–Ca²⁺ exchange

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Some Quantitative Aspects of the Relation of Rhythm to the Contractile Force of Mammalian Ventricular Muscle

Cited by 21 publications

References 0 publications

Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Potentiation of Myocardial Contractility by Continual Premature Extra-activations

Studies on Starling's Law of the Heart. Iii. Observations in Patients With Mitral Stenosis and Atrial Fibrillation on the Relationships Between Left Ventricular End-Diastolic Segment Length, Filling Pressure, and the Characteristics of Ventricular Contraction *

Excitation–contraction coupling in myocardium: implications of calcium release and Na+–Ca2+ exchange

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Excitation–contraction coupling in myocardium: implications of calcium release and Na⁺–Ca²⁺ exchange