Acute pressure overload cardiac arrhythmias are dependent on the presence of myocardial tissue catecholamines

Aj, Drake-Holland; Mi, Noble; Mj, Lab

doi:10.1136/heart.85.5.576

Cited by 15 publications

(2 citation statements)

References 45 publications

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“…In support of this signal chain, catecholamine store depletion curtails mechanoarrhythmia whether the depletion is pharmacological 30 or by chronic sympathetic denervation in the intact preparation 31 . This notion has been supported by a further study in the intact preparation 32…”

Section: At the Channel Levelmentioning

confidence: 86%

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

Lab

2006

Annals of the New York Academy of Sciences

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This review covers aspects of the cardiac mechanotransduction field at different levels, and advocates the possibility that mechanoelectro-chemical transduction forms part of a network of mechanically linked integration in heart-mechanically mediated integration (MMI). It assembles evidence and observations in the literature to promote this hypothesis. Mechanical components can provide the bond between interactions at molecular, cellular, and macro levels to enable the integration. Stretch-activated channels (SACs) exist in the heart, but stresses and strains can affect other membrane channels or receptors. A cellular mechanical change can thus promote several ionic or downstream changes. Cell signal cascades have been implicated and can affect membrane electrophysiology. MMI could shape intracellular and downstream signals using the cytoskeleton and intracellular Ca(2+). MMI also spans other regulatory systems and processes such as the autonomic nervous system (ANS) and operates throughout the whole heart as an integrative system. Finally, supporting the hypothesis, if elements of the normal integration become deranged it contributes to cardiovascular disease and, potentially, lethal arrhythmia.

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Section: At the Channel Levelmentioning

confidence: 86%

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

Lab

2006

Annals of the New York Academy of Sciences

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“…Other tissue types at the endocardial surface will be susceptible to Lugol, e.g., autonomic nerve terminals ( Drake-Holland et al, 2001 ), though the signalling pathways activated by stretch in these tissues is slower than the electrical response to stretch we describe. We conclude that, in accord with previous studies, the principal target of Lugol was the PF network, rather than the myocardium.…”

Section: Discussionmentioning

confidence: 84%

Attenuation of stretch-induced arrhythmias following chemical ablation of Purkinje fibres, in isolated rabbit hearts

et al. 2023

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Purkinje fibres (PFs) play an important role in some ventricular arrhythmias and acute ventricular stretch can evoke mechanically-induced arrhythmias. We tested whether Purkinje fibres, play a role in these arrhythmias. Pseudo-ECGs were recorded in isolated, Langendorff-perfused, rabbit hearts in which the left ventricular endocardial surface was also irrigated with Tyrode, via an indwelling catheter placed in the left ventricular lumen. The number and period of ectopic activations was measured during left ventricular lumen inflation via an indwelling fluid-filled balloon (500 μL added over 2 s and maintained for 15 s in total). Mechanically-induced arrhythmias occurred in 70% of balloon inflations: they were maximal in the first 5 s and ceased within 15 s. Brief, (10 s) irrigation of the left ventricular lumen with Lugol solution (IK/I2), via the indwelling catheter, reduced inflation-induced ectopics by 98% (p < 0.05). Ablation of endocardial PFs by Lugol was confirmed by Triphenyltetrazolium Chloride staining. Optical mapping revealed the left ventricular epicardial activation patterns of ectopics could have PF-mediated and focal sources. In silico modelling predicted ectopic sources originating in the endocardial region propagate to and through the Purkinje fibres network. Acute distention-induced ectopics are multi-focal, their attenuation by Lugol, their activation patterns and in silico modelling indicate a participation of Purkinje fibres in these arrhythmias.

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Mechanoelectric Transduction/Feedback: Physiology and Pathophysiology

Lab

Cardiac Mechanotransduction

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Acute pressure overload cardiac arrhythmias are dependent on the presence of myocardial tissue catecholamines

Cited by 15 publications

References 45 publications

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control

Attenuation of stretch-induced arrhythmias following chemical ablation of Purkinje fibres, in isolated rabbit hearts

Mechanoelectric Transduction/Feedback: Physiology and Pathophysiology

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