Ionic currents and action potentials in rabbit, rat, and guinea pig ventricular myocytes

Varró, András; Lathrop, David A.; Hester, S. B.; Nánási, P. P.; Papp, Julius Gyula

doi:10.1007/bf00798257

Cited by 130 publications

(13 citation statements)

References 30 publications

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“…These differences require repolarizing K + ionic currents with different kinetics in order to adapt the APD appropriately. In rats and mice, the major repolarizing K + ionic currents are the transient outward K + current (I to ) and ultra-rapid potassium current (I kur ), and the ventricular APD has a triangular shape, with short repolarization and no clear plateau phase ( Watanabe et al, 1983 ; Varró et al, 1993 ; Knollmann et al, 2001 ). Importantly, most rodent studies involve direct pacing under anesthesia, or ex-vivo / in-vitro preparations, overlooking the effects of autonomic stimulation.…”

Section: Myocardial Repolarization In Rats and Micementioning

confidence: 99%

Incorrectly corrected? QT interval analysis in rats and mice

Mulla

Murninkas²,

Levi³

et al. 2022

Front. Physiol.

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QT interval, a surrogate measure for ventricular action potential duration (APD) in the surface ECG, is widely used to identify cardiac abnormalities and drug safety. In humans, cardiac APD and QT interval are prominently affected by heart rate (HR), leading to widely accepted formulas to correct the QT interval for HR changes (QT corrected - QTc). While QTc is widely used in the clinic, the proper way to correct the QT interval in small mammals such as rats and mice is not clear. Over the years, empiric correction formulas were developed for rats and mice, which are widely used in the literature. Recent experimental findings obtained from pharmacological and direct pacing experiments in unanesthetized rodents show that the rate-adaptation properties are markedly different from those in humans and the use of existing QTc formulae can lead to major errors in data interpretation. In the present review, these experimental findings are summarized and discussed.

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Section: Myocardial Repolarization In Rats and Micementioning

confidence: 99%

Incorrectly corrected? QT interval analysis in rats and mice

Mulla

Murninkas²,

Levi³

et al. 2022

Front. Physiol.

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“…Specifically, varying expression and regulation of ion channels and transporters, notably K + channels (11)(12)(13)(14), are mechanistically associated with species-specific action potential (AP) properties. It has been shown, for example, that the presence of a more prominent "spike and dome" morphology is due to a large transient outward current I to in species like rabbit and human, while I to is virtually absent in the guinea pig, which lacks the AP notch (15). A much larger I to and expression of additional K + channels are responsible for the typical triangular AP shape and shorter AP duration (APD) in mouse and rat (versus nonrodents) ventricular myocytes (16).…”

Section: Introductionmentioning

confidence: 99%

Quantitative cross-species translators of cardiac myocyte electrophysiology: Model training, experimental validation, and applications

et al. 2021

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“…However, it is worth mentioning that canine experimental models have some limitations. First, the electrophysiological properties of animal cardiac tissue are different from human cardiac tissue 43 – 45 . Moreover, in experimental animal models BrS is pharmacologically induced in coronary perfused ventricular wedges, therefore reproducing the pathological substrate of the RVOT is challenging 46 .…”

Section: Discussionmentioning

confidence: 99%

Diffuse fibrosis and repolarization disorders explain ventricular arrhythmias in Brugada syndrome: a computational study

Biasi

Seghetti

Tognetti

2022

Sci Rep

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In this work, we reported a computational study to quantitatively determine the individual contributions of three candidate arrhythmic factors associated with Brugada Syndrome. In particular, we focused our analysis on the role of structural abnormalities, dispersion of repolarization, and size of the diseased region. We developed a human phenomenological model capable of replicating the action potential characteristics both in Brugada Syndrome and in healthy conditions. Inspired by physiological observations, we employed the phenomenological model in a 2D geometry resembling the pathological RVOT coupled with healthy epicardial tissue. We assessed the insurgence of sustained reentry as a function of electrophysiological and structural abnormalities. Our computational study indicates that both structural and repolarization abnormalities are essential to induce sustained reentry. Furthermore, our results suggest that neither dispersion of repolarization nor structural abnormalities are sufficient on their own to induce sustained reentry. It should be noted how our study seems to explain an arrhythmic mechanism that unifies the classic repolarization and depolarization hypotheses of the pathophysiology of the Brugada Syndrome. Finally, we believe that this work may offer a new perspective on the computational and clinical investigation of Brugada Syndrome and its arrhythmic behaviour.

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Ionic currents and action potentials in rabbit, rat, and guinea pig ventricular myocytes

Cited by 130 publications

References 30 publications

Incorrectly corrected? QT interval analysis in rats and mice

Incorrectly corrected? QT interval analysis in rats and mice

Quantitative cross-species translators of cardiac myocyte electrophysiology: Model training, experimental validation, and applications

Diffuse fibrosis and repolarization disorders explain ventricular arrhythmias in Brugada syndrome: a computational study

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