scholarly journals New Calculation of Internal Ca2+ Recirculation Fraction from Alternans Decay of Postextrasystolic Potentiation.

2001 ◽  
Vol 51 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Gentaro Iribe ◽  
Junichi Araki ◽  
Satoshi Mohri ◽  
Juichiro Shimizu ◽  
Takeshi Imaoka ◽  
...  
Keyword(s):  
Postextrasystolic Potentiation ◽  
Recirculation Fraction

Energy-wasteful total Ca2+ handling underlies increased O2 cost of contractility in canine stunned heart

2000 ◽  
Vol 278 (5) ◽  
pp. H1464-H1472 ◽  
Author(s):  
Shinyu Lee ◽  
Junichi Araki ◽  
Takeshi Imaoka ◽  
Masaki Maesako ◽  
Gentaro Iribe ◽  
...  
Keyword(s):  
Exponential Decay ◽  
Myocardial Stunning ◽  
Left Ventricular ◽  
Canine Heart ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Postextrasystolic Potentiation ◽  
Decay Component ◽  
Recirculation Fraction ◽  
Integrative Method

Postischemic myocardial stunning halved left ventricular contractility [end-systolic maximum elastance ( E max)] and doubled the O2 cost of E max in excised cross-circulated canine heart. We hypothesized that this increased O2 cost derived from energy-wasteful myocardial Ca2+ handling consisting of a decreased internal Ca2+ recirculation, some futile Ca2+ cycling, and a depressed Ca2+ reactivity of E max. We first calculated the internal Ca2+ recirculation fraction (RF) from the exponential decay component of postextrasystolic potentiation. Stunning significantly accelerated the decay and decreased RF from 0.63 to 0.43 on average. We then combined the decreased RF with the halved E maxand its doubled O2 cost and analyzed total Ca2+handling using our recently developed integrative method. We found a decreased total Ca2+ transport and a considerable shift of the relation between futile Ca2+ cycling and Ca2+ reactivity in an energy-wasteful direction in the stunned heart. These changes in total Ca2+ handling reasonably account for the doubled O2 cost of E max in stunning, supporting the hypothesis.

Temperature-dependent postextrasystolic potentiation and Ca2+ recirculation fraction in canine hearts

2002 ◽  
Vol 282 (2) ◽  
pp. H403-H413 ◽  
Author(s):  
Ju Mizuno ◽  
Junichi Araki ◽  
Shunsuke Suzuki ◽  
Satoshi Mohri ◽  
Takeshi Mikane ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Exponential Decay ◽  
Temperature Sensitivity ◽  
Systolic Pressure ◽  
Volume Ratio ◽  
Myocardial Cells ◽  
Temperature Dependent ◽  
Postextrasystolic Potentiation ◽  
Decay Component ◽  
Recirculation Fraction

We have found that cardiac temperature proportionally changes O2 cost of contractility, defined as O2 consumption for myocardial total Ca2+handling normalized to contractility in terms of the end-systolic pressure-volume ratio (maximal elastance, E max), in the canine left ventricle (temperature sensitivity, Q10 = 2). We have separately found that a decrease in the recirculation fraction (RF) of Ca2+ within myocardial cells underlies an increased O2 cost of E max in stunned hearts. We therefore hypothesized that a similar change in RF would underlie the Q10 of O2 cost of E max. We tested this hypothesis by analyzing RF calculated from an exponential decay component of the transiently alternating postextrasystolic potentiation in the canine left ventricle. RF decreased from 0.7 to 0.5 as cardiac temperature increased from 33 to 38°C with Q10 of 0.5, reciprocal to that of O2 cost of E max. We conclude that Q10 of ATP-consuming reactions involved in Ca2+handling and E max response to it could reasonably account for the reciprocal Q10 of RF and O2 cost of E max.

Postextrasystolic Potentiation During Spontaneous Ventricular Ectopy in Man

1984 ◽  
Vol 19 (5) ◽  
pp. 380-384 ◽  
Author(s):  
JOSEPH F. POLAK ◽  
B. LEONARD HOLMAN ◽  
PHILIP J. PODRID ◽  
BERNARD LOWN
Keyword(s):  
Ventricular Ectopy ◽  
Postextrasystolic Potentiation

Modeling short-term interval-force relations in cardiac muscle

2000 ◽  
Vol 278 (3) ◽  
pp. H913-H931 ◽  
Author(s):  
J. Jeremy Rice ◽  
M. Saleet Jafri ◽  
Raimond L. Winslow
Keyword(s):  
Ryanodine Receptor ◽  
Cell Model ◽  
Isometric Force ◽  
Delayed Rectifier ◽  
Short Term ◽  
Time Model ◽  
Receptor Adaptation ◽  
Myofilament Activation ◽  
Recirculation Fraction ◽  
Ventricular Cell Model

This study employs two modeling approaches to investigate short-term interval-force relations. The first approach is to develop a low-order, discrete-time model of excitation-contraction coupling to determine which parameter combinations produce the degree of postextrasystolic potentiation seen experimentally. Potentiation is found to increase 1) for low recirculation fraction, 2) for high releasable fraction, i.e., the maximum fraction of Ca2+released from the sarcoplasmic reticulum (SR) given full restitution, and 3) for strong negative feedback of the SR release on sarcolemmal Ca2+ influx. The second modeling approach is to develop a more detailed single ventricular cell model that simulates action potentials, Ca2+-handling mechanisms, and isometric force generation by the myofilaments. A slow transition from the adapted state of the ryanodine receptor produces a gradual recovery of the SR release and restitution behavior. For potentiation, a small extrasystolic release leaves more Ca2+ in the SR but also increases the SR loading by two mechanisms: 1) less Ca2+-induced inactivation of L-type channels and 2) reduction of action potential height by residual activation of the time-dependent delayed rectifier K+ current, which increases Ca2+ influx. The cooperativity of the myofilaments amplifies the relatively small changes in the Ca2+ transient amplitude to produce larger changes in isometric force. These findings suggest that short-term interval-force relations result mainly from the interplay of the ryanodine receptor adaptation and the SR Ca2+ loading, with additional contributions from membrane currents and myofilament activation.

Postextrasystolic potentiation echocardiography in predicting reversible myocardial dysfunction by surgical coronary revascularization

1998 ◽  
Vol 81 (12) ◽  
pp. 36G-40G ◽  
Author(s):  
Roldano Scognamiglio ◽  
Marco Marin ◽  
Manuela Miorelli ◽  
Monica Palisi ◽  
Giuseppe Fasoli ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Coronary Revascularization ◽  
Postextrasystolic Potentiation

Rhythm effects on contractility of the beating isovolumic left ventricle

1960 ◽  
Vol 199 (6) ◽  
pp. 1115-1120 ◽  
Author(s):  
B. Lendrum ◽  
H. Feinberg ◽  
E. Boyd ◽  
L. N. Katz
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Ventricular Volume ◽  
Contractile Force ◽  
Postextrasystolic Potentiation ◽  
Pressure Development ◽  
Induced Changes ◽  
Electrical Alternans

Variation in contractile force of the isovolumic contracting left ventricle of the dog was studied in open-chested in situ hearts. The electrocardiogram and intraventricular pressures were recorded at various heart volumes. Spontaneous changes in heart rate and rhythm occurred at all volumes. Isovolumic systolic pressure development (contractile force) varied with rate and rhythm. Contractile force increased with heart rate (treppe) regardless of pacemaker origin. When a premature beat was followed by a compensatory pause, the premature beat showed a decrease and the next beat an increase in contractile force (postextrasystolic potentiation). The magnitude of the changes varied directly with the prematurity of the beat. Mechanical alternans was observed with electrical alternans, despite the absence of significant volume change. Rate-induced changes, postextrasystolic potentiation and mechanical alternans were additive when they occurred simultaneously. For practical purposes, ventricular volume (filling), hence muscle fiber length, remained constant during these rate and rhythm change, therefore could not affect the strength of contraction. Contractile force changes directly attributable to rate and rhythm changes do, therefore, occur in the intact mammalian heart.

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