Length-dependent changes in myocardial contractile state

Parmley, W.W.; Chuck, Leonard

doi:10.1152/ajplegacy.1973.224.5.1195

Cited by 176 publications

(114 citation statements)

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“…Elevation of the muscle bath temperature was found to increase, 49 have no effect on, 55 or decrease 57 mum difference but decreased it in the force region between 0.5 and 2 g. 55 The discrepancy may be a consequence of a variable degree of facilitatory effect of previous shortening contractions 58 " 60 and/or a variability in the long-term effect of change in preload length. 61 This long-term historydependent behavior (which develops over many minutes) presents a real difficulty in the precise quantification of mode-dependent differences in the end-systolic F-L relation (i.e., short-term history dependence). An extremely careful experimental design becomes necessary, including control of the number of beats after each change in contraction mode as well as in the range and direction of alteration of muscle length.…”

Section: End-systolic* Force-length Relationmentioning

confidence: 99%

The ventricular pressure-volume diagram revisited.

Sagawa¹

1978

Circulation Research

450

134

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Section: End-systolic* Force-length Relationmentioning

confidence: 99%

The ventricular pressure-volume diagram revisited.

Sagawa¹

1978

Circulation Research

450

134

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“…Myocardial contractility is regulated via force-length relation (Frank-Starling Law for whole heart) that links a maximal isometric force with a degree of muscle stretch or preload [1]. It is well established that an increase of preload in the physiological range results in an increase of peak isometric force or afterload shortening, a rise of maximal rates of force development and relaxation as well as time-to-peak tension and relaxation time.…”

Section: Introductionmentioning

confidence: 99%

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

Lookin

Protsenko

2011

Open Life Sciences

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Preload-induced changes of active tension and [Ca2+]i are “dissociated” in mammalian myocardium. This study aimed to describe the distinct effects of preload at low and physiological [Ca2+]o. Rat RV papillary muscles were studied in isometric conditions at 25‡C and 0.33 Hz at 1 mM (hypo-Ca group) and 2.5 mM [Ca2+]o (normal-Ca group). [Ca2+]i was monitored with fura-2/AM. Increase of preload caused a rise of active tension in hypo-Ca and normal-Ca groups whereas peak fluorescence rose significantly only at low [Ca2+]o. End-diastolic tension, end-diastolic level of fluorescence, time-to-peak tension, but not time-to-peak of Ca2+ transient, progressively increased with preload. Mechanical relaxation decelerated with preload while Ca2+ transient decay time decreased in the initial phase and increased in the late phase, resulting in a prominent “bump” configuration. The “bump” was assessed as a ratio of its area to the fluorescence trace area. It was a new finding that the preload-induced rise of this ratio was twice as large in hypo-Ca. Our results indicate that preload-induced changes in active tension and [Ca2+]i are “dissociated” in rat myocardium, with relatively higher expression at low [Ca2+]o. Ca-dependence of Ca-TnC association/dissociation kinetics is thought to be a main contributor to these preload-induced effects.

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“…The SFR was originally characterised in cat papillary muscles (Parmley and Chuck, 1973). Since then, it has been observed in a variety of cardiac preparations ranging from whole hearts to single myocytes in various species including cat (Parmley and Chuck, 1973;Perez et al, 2001), dog (Todaka et al, 1998), ferret (Calaghan and White, 2001), guineapig (White et al, 1995), rabbit (von Lewinski et al, 2003), rat (Alvarez et al, 1999;Hongo et al, 1996;Kentish and Wrzosek, 1998), and human (von Lewinski et al, 2004). This implicates that the SFR is a general phenomenon of physiological relevance and that the underlying mechanisms of the SFR, just like the FSM, are intrinsic to the cardiac myocyte.…”

Section: Introductionmentioning

confidence: 99%

The slow force response to stretch in atrial and ventricular myocardium from human heart: Functional relevance and subcellular mechanisms

Kockskämper

Lewinski

Khafaga

et al. 2008

Progress in Biophysics and Molecular Biology

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Mechanical load is an important regulator of cardiac force. Stretching human atrial and ventricular trabeculae elicited a biphasic force increase: an immediate increase (Frank-Starling mechanism) followed by a further slow increase (slow force response, SFR). In ventricle, the SFR was unaffected by AT-and ET-receptor antagonism, by inhibition of protein-kinase-C, PI-3-kinase, and NOsynthase, but attenuated by inhibition of Na + /H + -(NHE) and Na + /Ca 2+ -exchange (NCX). In atrium, however, neither NHE-nor NCX-inhibition affected the SFR. Stretch elicited a large NHE-dependent [Na + ] i increase in ventricle but only a small, NHE-independent [Na + ] i increase in atrium. Stretchactivated non-selective cation channels contributed to basal force development in atrium but not ventricle and were not involved in the SFR in either tissue. Interestingly, inhibition of AT-receptors or pre-application of angiotensin II or endothelin-1 reduced the atrial SFR. Furthermore, stretch increased phosphorylation of atrial myosin light chain 2 (MLC2) and inhibition of myosin light chain kinase (MLCK) attenuated the SFR in atrium and ventricle. Thus, in human heart both atrial and ventricular myocardium exhibit a stretch-dependent SFR that might serve to adjust cardiac output to increased workload. In ventricle, there is a robust NHE-dependent (but angiotensin II-and endothelin-1-independent) [Na + ] i increase that is translated into a [Ca 2+ ] i and force increase via NCX. In atrium, on the other hand, there is an angiotensin II-and endothelin-dependent (but NHE-and NCX-independent) force increase. Increased myofilament Ca 2+ sensitivity through MLCK-induced phosphorylation of MLC2 is a novel mechanism contributing to the SFR in both atrium and ventricle.

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Length-dependent changes in myocardial contractile state

Cited by 176 publications

References 0 publications

The ventricular pressure-volume diagram revisited.

The ventricular pressure-volume diagram revisited.

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

The slow force response to stretch in atrial and ventricular myocardium from human heart: Functional relevance and subcellular mechanisms

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