Model of calcium movements in the mammalian myocardium: Interval-strength relationship

Adler, David; Wong, Alan Y.K.; Mahler, Y.; Klassen, Gerald A.

doi:10.1016/s0022-5193(85)80233-2

Cited by 35 publications

(26 citation statements)

References 25 publications

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“…Aside from the classic 1975 papers by Bass (3, 4), which described the two phases of electromechanical restitution in cat papillary muscles, most investigations have focused on phase II, specifically on that portion of phase II that follows complete relaxation of the steady-state beat (1,36,40). In such studies, there typically are mathematical extrapolations to zero developed force or zero intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) transient amplitude as the ESI is shortened; fused waveforms are not dealt with (36).…”

Section: Discussionmentioning

confidence: 99%

“…This reversal point can be taken as the boundary between phase I and phase II, but there undoubtedly is functional overlap, with the process(es) responsible for phase II possibly beginning near the extrapolated value for T 0 . Mechanical restitution and other aspects of the myocardial strength-interval relation (1,24,33) may reflect 1) changes in the gating mode of the L-type Ca 2ϩ channels (dihydropyridine receptors, DHPRs) (29,33); 2) changes in the extent to which Ca 2ϩ release channels (ryanodine receptors, RyRs) of the sarcoplasmic reticulum (SR) recover the ability to release Ca 2ϩ (34); 3) alterations in the amount of Ca 2ϩ contained in the SR (6); and 4) cross-talk between the RyRs and the DHPRs wherein Ca 2ϩ influx via the L-type Ca 2ϩ channels triggers SR Ca 2ϩ release and Ca 2ϩ released from the SR inactivates the DHPRs (6). Each of these processes appears to be highly regulated and offers a potential target for therapeutic modalities designed to improve electromechanical function in diseased hearts.…”

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confidence: 99%

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Phase I and phase II of short-term mechanical restitution in perfused rat left ventricles

Dumitrescu

Narayan

Cheng

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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. Phase I and phase II of short-term mechanical restitution in perfused rat left ventricles. Am J Physiol Heart Circ Physiol 282: H1311-H1319, 2002. First published December 6, 2001 10.1152/ajpheart.00464.2001.-We examined the contributions of the Ca 2ϩ channels of the sarcolemma and of the sarcoplasmic reticulum to electromechanical restitution. Extrasystoles (F 1) were interpolated 40-600 ms following a steady-state beat (F 0) in perfused rat ventricles paced at 2 or 3 Hz. Plots of F 1/F0 versus the extrasystolic interval consisted of phase I, which occurred before relaxation of the steady-state beat, and phase II, which occurred later. Phase I exhibited a period of enhanced left ventricular pressure development that coincided with action potential prolongation. Phase I was eliminated by ϪBAY K 8644 (100 nM) and FPL 64176 (150 nM), augmented by 3 M thapsigargin plus 200 nM ryanodine and unaffected by KN-93 and KB-R7943. Phase II was accelerated by the Ca 2ϩ channel agonists and by isoproterenol but was eliminated by thapsigargin plus ryanodine. The results suggest that phase I of electromechanical restitution is caused by a transient L-type Ca 2ϩ current facilitation, whereas phase II represents the recovery of the ability of the sarcoplasmic reticulum to release Ca 2ϩ .L-type calcium channels; sarcoplasmic reticulum; ryanodine receptors; myocardium; calmodulin MECHANICAL RESTITUTION is the time-dependent recovery of the ability of the heart to contract following the previous beat. That is, a premature stimulus or extrasystole introduced soon after the relaxation of a steadystate beat produces an attenuated twitch, the amplitude of which depends on the duration of the extrasystolic interval (ESI) (36). As the interval between the relaxation of a steady-state beat and the extrasystole is increased, there is an exponential increase in the amplitude of the extrasystolic beat. In fact, as the interval is prolonged beyond that of the basic cycle length, the twitch amplitude continues to increase and becomes greater than that of the steadystate beat before reaching a plateau (36). In 1975, Bass (3) termed this monoexponential recovery of force or pressure development phase II of mechanical restitution. He noted that when extrasystoles are interpolated very early and before relaxation of the steady-state beat, there is a period of enhanced relative force development (phase I) that is accompanied by action potential prolongation (4). The phase I enhancement of force development declines with increasing extrasystolic intervals, reaching a minimum value or reversal point (3). This reversal point can be taken as the boundary between phase I and phase II, but there undoubtedly is functional overlap, with the process(es) responsible for phase II possibly beginning near the extrapolated value for T 0 . Mechanical restitution and other aspects of the myocardial strength-interval relation (1, 24, 33) may reflect 1) changes in the gating mode of the L-type Ca 2ϩ channels (dihydropyridine receptors, DHPRs) (29, 33); 2) changes...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Phase I and phase II of short-term mechanical restitution in perfused rat left ventricles

Dumitrescu

Narayan

Cheng

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…By modifying the numerical values of parameters of constants in Fig. 2, the free Ca 2+ in RT can be limited to about 18 µM (Adler et al, 1985). (2) Considering the MCS as the compartment which can store, release and sequester Ca 2+ , then LSR is not necessary.…”

Section: Discussionmentioning

confidence: 99%

“…In other words, it is necessary to assume a high free Ca 2 in the MCS during resting state, as in the other E-C coupling models (Cannell and Allen, 1984;Adler et al, 1985). If the free Ca 2+ in the MCS were high, calcium would be extruded continuously across the SR membrane to the outside diffusion.…”

Section: Discussionmentioning

confidence: 99%

Model of calcium-induced calcium release mechanism in cardiac cells

Wong

Fabiato

Bassingthwaighthe

1992

Bltn Mathcal Biology

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A model with which to elucidate the mechanism of Ca 2+ release from, and Ca 2+ loading in the sarcoplasmic reticulum (SR) by Ca 2+ current (I Ca ) in cardiac cells is proposed. The SR is assumed to be comprised of three functional subcompartments: (1) the main calcium store (MCS), which contains most of the calcium (both free and bound); (2) the releasable terminal (RT), which contains the calcium readily available for release; and (3) the longitudinal network of the SR (LSR), which sequesters and the transfers the sarcoplasmic calcium to the RT. A rapid increase of the Ca 2+ concentration at the outer surface of the SR (Ca e ) due to the fast component of I Ca activates and inactivates this surface, inducing the release of Ca 2+ from the RT to the sarcoplasmic space. The RT in turn is further activated and inactivated by a increase in the concentration of sarcoplasmic Ca 2+ . The Ca 2+ in the sarcoplasmic space is then sequestered by the LSR, leading to the reactivation of the RT. Further increase of Ca e due to the slow component of I Ca enhances the entry of Ca 2+ into the MCS to be bound by the binding substance. The free Ca 2+ released from the Ca-binding substance complex is transferred to the RT for subsequent release. The activation, inactivation and reactivation are Ca 2+ -mediated and time-dependent. The proposed model yields simulation of the many events qualitatively similar to those observed experimentally in skinned cardiac cells.

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“…Ca 2+ handling model. The conventional monotonic or exponential PESP decay has been accounted for by the beat-by-beat decreasing Ca 2+ release in E-C coupling from its once transiently augmented level in PES1 toward the steady-state level of the regular beats [1][2][3][29][30][31][32][33][34]. The most potentiated PES1 is considered to be due to both the increased transsarcolemmal Ca 2+ influx and the increased Ca 2+ released from SR because of the disturbed Ca 2+ homeostasis [1][2][3].…”

Section: Methodsmentioning

confidence: 99%

Load Independence of Temperature-Dependent Ca2+ Recirculation Fraction in Canine Heart

Mizuno

Mohri

Shimizu

et al. 2004

JJP

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Model of calcium movements in the mammalian myocardium: Interval-strength relationship

Cited by 35 publications

References 25 publications

Phase I and phase II of short-term mechanical restitution in perfused rat left ventricles

Phase I and phase II of short-term mechanical restitution in perfused rat left ventricles

Model of calcium-induced calcium release mechanism in cardiac cells

Load Independence of Temperature-Dependent Ca2+ Recirculation Fraction in Canine Heart

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