Force-Frequency-Relation in Human Atrial and Ventricular Myocardium

Background In human ventricular myocardium, contractile force increases at higher stimulation frequencies (positive force-frequency relation). In failing hearts, the force-frequency relation (FFR) is negative. Data on the effect of volatile anesthetics on FFR are very limited. Methods The authors obtained left ventricular tissue from 18 explanted hearts from patients undergoing cardiac transplantation and tissue of 8 organ donors. The negative inotropic effect of halothane, isoflurane, and sevoflurane on isometric force of contraction of isolated muscle preparations at a stimulation frequency of 1 and 3 Hz and the effect of each anesthetic on the FFR were studied. Ryanodine and verapamil were studied for comparison. In addition, the effect of the anesthetics on Ca(2+)-dependent (3)H-ryanodine binding was investigated. Results In nonfailing myocardium, halothane was the strongest negative inotropic compound, and the positive FFR was not affected by either drug. In failing myocardium, halothane also showed the strongest negative inotropic effect, but the positive shape of FFR was restored by halothane and ryanodine. In contrast, isoflurane, sevoflurane, and verapamil did not change FFR. Only halothane shifted the Ca(2+)-dependent (3)H-ryanodine binding curve toward lower Ca(2+) concentrations. Conclusion In nonfailing human myocardium, none of the anesthetics affect FFR, but halothane is the strongest negative inotropic compound. In failing myocardium, halothane, but not isoflurane or sevoflurane, restores the positive shape of FFR. Both the more pronounced negative inotropic effect of halothane and the restoration of the positive shape of FFR in failing myocardium in the presence of halothane can be explained by its interaction with the myocardial sarcoplasmic reticulum calcium-release channel.

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Force-frequency-relation in human atrial and ventricular myocardium

Molecular and Cellular Biochemistry ◽

10.1007/bf00926856 ◽

1993 ◽

Vol 119 (1-2) ◽

pp. 73-78 ◽

Cited By ~ 18

Author(s):

Robert H. G. Schwinger ◽

Michael B�hm ◽

Andrea Koch ◽

Rainer Uhlmann ◽

Peter �berfuhr ◽

...

Keyword(s):

Ventricular Myocardium ◽

Force Frequency ◽

Frequency Relation

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Ca2+ handling in isolated human atrial myocardium

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.3.h952 ◽

2000 ◽

Vol 279 (3) ◽

pp. H952-H958 ◽

Cited By ~ 28

Author(s):

Lars S. Maier ◽

Paul Barckhausen ◽

Jutta Weisser ◽

Ivo Aleksic ◽

Mersa Baryalei ◽

...

Keyword(s):

Mechanical Performance ◽

Ventricular Myocardium ◽

Force Frequency ◽

Atrial Myocardium ◽

Twitch Force ◽

Intracellular Ca ◽

Beating Rate ◽

Frequency Relation ◽

Isometric Twitch ◽

Rest Intervals

Physiologically, human atrial and ventricular myocardium are coupled by an identical beating rate and rhythm. However, contractile behavior in atrial myocardium may be different from that in ventricular myocardium, and little is known about intracellular Ca2+handling in human atrium under physiological conditions. We used rapid cooling contractures (RCCs) to assess sarcoplasmic reticulum (SR) Ca2+ content and the photoprotein aequorin to assess intracellular Ca2+ transients in atrial and ventricular muscle strips isolated from nonfailing human hearts. In atrial myocardium ( n = 19), isometric twitch force frequency dependently (0.25–3 Hz) increased by 78 ± 25% (at 3 Hz; P < 0.05). In parallel, aequorin light signals increased by 111 ± 57% ( P < 0.05) and RCC amplitudes by 49 ± 13% ( P < 0.05). Similar results were obtained in ventricular myocardium ( n = 13). SR Ca2+ uptake (relative to Na+/Ca2+ exchange) frequency dependently increased in atrial and ventricular myocardium ( P < 0.05). With increasing rest intervals (1–240 s), atrial myocardium ( n = 7) exhibited a parallel decrease in postrest twitch force (at 240 s by 68 ± 5%, P < 0.05) and RCCs (by 49 ± 10%, P < 0.05). In contrast, postrest twitch force and RCCs significantly increased in ventricular myocardium ( n = 6). We conclude that in human atrial and ventricular myocardium the positive force-frequency relation results from increased SR Ca2+ turnover. In contrast, rest intervals in atrial myocardium are associated with depressed contractility and intracellular Ca2+ handling, which may be due to rest-dependent SR Ca2+ loss (Ca2+ leak) and subsequent Ca2+ extrusion via Na+/Ca2+ exchange. Therefore, the influence of rate and rhythm on mechanical performance is not uniform in atrial and ventricular myocardium.

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Force-frequency relation and myofilament Ca2+ sensitivity

10.36866/pn.71.39 ◽

2008 ◽

pp. 39-41

Author(s):

Regis Lamberts ◽

Jolanda van der Velden ◽

Ger Stienen

Keyword(s):

Force Frequency ◽

Frequency Relation

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Adrenergic Control of the Force-Frequency Relation

Circulation ◽

10.1161/01.cir.92.8.2327 ◽

1995 ◽

Vol 92 (8) ◽

pp. 2327-2332 ◽

Cited By ~ 92

Author(s):

John Ross ◽

Toshiro Miura ◽

Masashi Kambayashi ◽

Gregory P. Eising ◽

Kyu-Hyung Ryu

Keyword(s):

Force Frequency ◽

Adrenergic Control ◽

Frequency Relation

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Heart rate as a determinant of L-type Ca2+ channel activity: Mechanisms and implication in force-frequency relation

Basic Research in Cardiology ◽

10.1007/pl00007389 ◽

1998 ◽

Vol 93 (S1) ◽

pp. s051-s059 ◽

Cited By ~ 10

Author(s):

S. Lemaire ◽

C. Piot ◽

F. Leclercq ◽

V. Leuranguer ◽

J. Nargeot ◽

...

Keyword(s):

Heart Rate ◽

Force Frequency ◽

Channel Activity ◽

Frequency Relation

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Dynamic control of maximal ventricular elastance via the baroreflex and force-frequency relation in awake dogs before and after pacing-induced heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00922.2009 ◽

2010 ◽

Vol 299 (1) ◽

pp. H62-H69 ◽

Cited By ~ 5

Author(s):

Xiaoxiao Chen ◽

Javier A. Sala-Mercado ◽

Robert L. Hammond ◽

Masashi Ichinose ◽

Soroor Soltani ◽

...

Keyword(s):

Heart Failure ◽

Transfer Function ◽

Transfer Functions ◽

Dynamic Properties ◽

System Response ◽

Force Frequency ◽

Arterial Baroreflex ◽

Ventricular Elastance ◽

Arterial Blood ◽

Frequency Relation

We investigated to what extent maximal ventricular elastance ( Emax) is dynamically controlled by the arterial baroreflex and force-frequency relation in conscious dogs and to what extent these mechanisms are attenuated after the induction of heart failure (HF). We mathematically analyzed spontaneous beat-to-beat hemodynamic variability. First, we estimated Emax for each beat during a baseline period using the ventricular unstressed volume determined with the traditional multiple beat method during vena cava occlusion. We then jointly identified the transfer functions (system gain value and time delay per frequency) relating beat-to-beat fluctuations in arterial blood pressure (ABP) to Emax (ABP→ Emax) and beat-to-beat fluctuations in heart rate (HR) to Emax (HR→ Emax) to characterize the dynamic properties of the arterial baroreflex and force-frequency relation, respectively. During the control condition, the ABP→ Emax transfer function revealed that ABP perturbations caused opposite direction Emax changes with a gain value of −0.023 ± 0.012 ml−1, whereas the HR→ Emax transfer function indicated that HR alterations caused same direction Emax changes with a gain value of 0.013 ± 0.005 mmHg·ml−1·(beats/min)−1. Both transfer functions behaved as low-pass filters. However, the ABP→ Emax transfer function was more sluggish than the HR→ Emax transfer function with overall time constants (indicator of full system response time to a sudden input change) of 11.2 ± 2.8 and 1.7 ± 0.5 s ( P < 0.05), respectively. During the HF condition, the ABP→ Emax and HR→ Emax transfer functions were markedly depressed with gain values reduced to −0.0002 ± 0.007 ml−1 and −0.001 ± 0.004 mmHg·ml−1·(beats/min)−1 ( P < 0.1). Emax is rapidly and significantly controlled at rest, but this modulation is virtually abolished in HF.

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