Effect of ischemia on calcium-dependent fluorescence transients in rabbit hearts containing indo 1. Correlation with monophasic action potentials and contraction.

Lee, Hon-Chi; Mohabir, Rajendra; Smith, Nellis A.; Franz, Michael R.; Clusin, William T.

doi:10.1161/01.cir.78.4.1047

Cited by 257 publications

(132 citation statements)

References 43 publications

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“…31 The alternans in the calciumdependent fluorescence transient was also reported in ischemic rabbit hearts. 32 In this study, however, treatment with verapamil did not suppress the ST a . This suggested that the other mechanism may work on the flecainide-induced ST a .…”

Section: Mechanism Of St a Due To Flecainidecontrasting

confidence: 65%

Intracoronary Flecainide Induces ST Alternans and Reentrant Arrhythmia on Intact Canine Heart

et al. 1999

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Section: Mechanism Of St a Due To Flecainidecontrasting

confidence: 65%

Intracoronary Flecainide Induces ST Alternans and Reentrant Arrhythmia on Intact Canine Heart

et al. 1999

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“…Although the mechanism underlying alternans is not completely understood, alternations in contractile force are thought to result from variations in intracellular calcium release. 8 Additional evidence of impaired SR function at increasing stimulation rates with heart failure reported by other investigators 1 ' 2 ' 6 are fusion of Ught transients and contraction with increases in both enddiastolic intracellular calcium concentration and end-diastolic tone and a decrease in peak active tension development. Under the same conditions, control muscle preparations did not exhibit fusion or a decline in the force of contraction.…”

Section: -32mentioning

confidence: 76%

Effects of treppe and calcium on intracellular calcium and function in the failing heart from the spontaneously hypertensive rat.

Brooks¹,

Bing²,

Litwin³

et al. 1994

Hypertension

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We studied functional and intracellular calcium responses to treppe and extracellular calcium in spontaneously hypertensive rat (SHR) hearts during the transition from compensated pressure overload to failure. Intracellular calcium was measured using aequorin, a bioluminescent Ca 2+ indicator. Experiments were performed with intact, isovolumically contracting, buffer-perfused hearts from three rat groups: (1) aging SHR with evidence of heart failure (SHR-F), (2) age-matched SHR with no evidence of heart failure (SHR-NF), and (3) age-matched normotensive Wistar-Kyoto (WKY) rats. In each experiment, left ventricular pressure and intracellular calcium transients were simultaneously recorded. Hearts were studied at 30°C and paced at a rate of 1.6 Hz while being perfused with oxygenated Krebs-Henseleit solution (95% O 2 /5% CO 2 ) at 100 mm Hg. At the baseline state, peak systolic pressure was greatest in the SHR-NF group and lowest in the SHR-F group. Peak and resting [Ca 2+ ]i were not significantly different among groups; however, the calcium transient was prolonged in the SHR-NF and SHR-F groups. With increasing perfusate [Ca 2+ ] o from 0.5 to 3.0 mmol/L, the relative increases in peak [Ca 2+ ]| and peak systolic pressure were similar among groups. When stimulation rate was increased from 1.6 to 2.0, 2.4, 2.8, and 3.2 Hz, peak [Ca 2+ ]i, peak R elatively few models of cardiac pressure overload have stable hypertrophy persisting over most of the animal's life followed by a state in which chamber and muscle function are impaired. The spontaneously hypertensive rat (SHR) is a model that in many respects parallels the course of human hypertensive heart disease. Studies of both failing human 13 ], and pressure decrease in parallel in the SHR-F heart with increasing stimulation rate, suggesting that impaired calcium cycling may contribute to compromised pump function in the SHR-F heart. (Hypertension. 1994^4J47-356.) Keywords • calcium • heart hypertrophy muscle, cardiac heart failure, congestive in the force-frequency response between failing and nonfailing human myocardia and a reduced ability of the failing heart to increase force at increasing stimulation rates.6 Studies of isolated ventricular strips from failing human ventricles demonstrate that increased stimulation rates enhance disturbances in calcium handling 1 ' 2 and force development.6 It is well recognized that treppe and increasing [Ca 2+ ] o lead to an increase in [Ca 2+ ], and the number of occupied crossbridges per unit time, which in turn results in an increase in myocardial energy demands. In addition, both of these interventions lead to increases in [Ca 2+ ], and a greater load on intracellular calcium control systems. However, one problem with isolated muscle studies is the uncertainty regarding diffusion, inherent in isolated muscle studies, and the applicability to in vivo physiology. To bridge the gap between isolated muscle studies and in vivo physiology, we have carried out studies in the isolated perfused heart prepa...

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“…There are several reports of electrical-mechanical discordance under disease conditions. For example, Lee et al (1988) have shown electrical-mechanical discordance (short APD associated with large calcium transient) in ischemic hearts. Murphy et al (1994) have also shown electrical-mechanical discordant alternans, but in normal Landrace pigs that were paced rapidly.…”

Section: Voltage and Calcium Couplingmentioning

confidence: 99%

Cellular mechanisms of arrhythmogenic cardiac alternans

Laurita

Rosenbaum

2008

Progress in Biophysics and Molecular Biology

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Mechanical dysfunction remains as one of the best predictors of sudden cardiac death (SCD), but despite this close association the causal relationships between electrical instability and mechanical dysfunction are not fully understood. (Bigger et al., 1984;Buxton et al., 1984) Even though the effects of electrical instability on mechanical dysfunction of the heart is well appreciated and relatively clear, the reverse effects that mechanical dysfunction have electrical instability, or mechano-electrical feedback (MEF), are not. (Kohl et al., 2006;Lab, 1996) Stretch activated channels, for example, are one way mechanical activity can directly influence electrical activity at the cellular level under physiologic and pathophysiological conditions. (Hu et al., 1997) Alternatively, intracellular calcium, which regulates mechanical contraction, can significantly influence electrical function of the heart as well. The mechanisms by which intracellular calcium governs electrical instability of the heart is the main focus of this manuscript. Traditionally, calcium mediated arrhythmogenesis is associated with delayed after depolarizations and abnormal impulse formation. (Katra et al., 2007;Liu et al., 2006;Rosen, 1985;Ter Keurs et al., 2006;Wehrens et al., 2003) However, in this manuscript we focus on how cardiac alternans, a mechanisms of reentrant excitation, is another significant way mechanical dysfunction and arrhythmogenesis are causally related.Cardiac alternans can refer to either mechanical (contractile) or electrical (repolarization) oscillations that occur on an every other beat basis. Cardiac alternans has been recognized for more than 100 years. Shown in Figure 1 (Panel A) is a very early record of arterial pressure measured during a steady state heart rate, where pulse magnitude alternates on every other beat (arrows). (Traube, 1872) At this time, the ECG had not been invented; however, soon after its introduction electrical alternans was reported as well. Shown in Panel B (Figure 1) is an early example of electrical alternans as evidenced by oscillations of the ECG T-wave (arrows) and QRS. (Lewis, 1910) Soon after cardiac alternans was first reported, it was associated with a poor prognosis. (Windle, 1913) Surprisingly, at this same time several important characteristics of cardiac alternans were observed, such as alternans occurring in a structurally normal heart and appearing at faster heart rates. Subsequently, Twave alternans was more directly related to coronary artery occlusion and shown to be highly reproducible. (Hellerstein et al., 1950)

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Effect of ischemia on calcium-dependent fluorescence transients in rabbit hearts containing indo 1. Correlation with monophasic action potentials and contraction.

Cited by 257 publications

References 43 publications

Intracoronary Flecainide Induces ST Alternans and Reentrant Arrhythmia on Intact Canine Heart

Intracoronary Flecainide Induces ST Alternans and Reentrant Arrhythmia on Intact Canine Heart

Effects of treppe and calcium on intracellular calcium and function in the failing heart from the spontaneously hypertensive rat.

Cellular mechanisms of arrhythmogenic cardiac alternans

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