Ectopic Pacemaker Activity
Ectopic Pacemaker Activity - Related Videos
16:19
Localized RNAi and Ectopic Gene Expression in the Medicinal Leech
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Cited by 5 •
2008
In this video, we show a procedure for an accurate biolistic delivery of reagents into live tissue with a novel miniature gene gun. We are knocking down the expression of the axon guidance molecule Netrin in leech embryos by delivering molecules of dsRNA into the ventral body wall and ganglia of single segments.
08:52
Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection
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Cited by 13 •
2015
This protocol describes how to produce functional sinus nodal tissue from murine pluripotent stem cells (PSC). T-Box3 (TBX3) overexpression plus cardiac Myosin-heavy-chain (Myh6) promoter antibiotic selection leads to highly pure pacemaker cell aggregates. These “Induced-sinoatrial-bodies” (“iSABs”) contain over 80% pacemaker cells, show highly increased beating rates and are able to pace myocardium ex vivo.
10:02
An Ectopic Chemokine Expression Model for Testing Macrophage Recruitment In Vivo
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2019
To test the effect of a chemokine on macrophage recruitment in vivo, the whole mount in situ hybridization was used to detect the ectopic expression of the chemokine, and immunostaining was used to label macrophages. Live imaging was used for real-time observation of macrophage migration.
07:38
Isolating and Imaging Live, Intact Pacemaker Regions of Mouse Renal Pelvis by Vibratome Sectioning
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Cited by 1 •
2021
The goal of this protocol is to isolate intact pacemaker regions of the mouse renal pelvis using vibratome sectioning. These sections can then be used for in situ Ca2+ imaging to elucidate Ca2+ transient properties of pacemaker cells and other interstitial cells in vibratome slices.
09:20
Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Cited by 2 •
2021
This protocol aims to describe a new methodology to measure intrinsic cardiac firing rate using microelectrode array recording of the whole sinoatrial node tissue to identify pacemaking defects in mice. Pharmacological agents can also be introduced in this method to study their effects on intrinsic pacemaking.
FAQs
Abnormal automaticity reflects an altered phase 4 depolarization, allowing nonpacemaker cells to gradually move toward threshold without a preceding impulse. Triggered activity instead depends on afterdepolarizations, which are abnormal voltage changes associated with prior electrical activity. This distinction matters pharmacologically because the responsible ion-current abnormality can influence which antiarrhythmic strategy is most appropriate.
Afterdepolarizations can push cardiac cells to threshold when ion-channel function is disturbed, creating an additional impulse at an inappropriate time. Their significance lies in converting an electrical disturbance into repetitive or premature activity that can disrupt rhythm. Understanding this mechanism helps explain why treatments targeting sodium, calcium, or potassium currents may suppress certain arrhythmic patterns.
These conditions can alter the electrical behavior of cardiac cells and make threshold easier to reach outside the normal pacemaking site. Ischemia and electrolyte disturbances affect the cellular environment, while autonomic stimulation changes sympathetic influence on cardiac excitability. Together, they increase the likelihood that abnormal automaticity or triggered activity will generate premature impulses or tachyarrhythmias.
Antiarrhythmic drugs can reduce ectopic firing by modifying sodium, calcium, or potassium currents, thereby changing the electrical conditions that support depolarization and threshold attainment. Some treatments also influence sympathetic activity, addressing an autonomic contribution to abnormal excitability. These actions provide a pharmacological basis for suppressing premature beats and tachyarrhythmias.
The mechanism helps connect a rhythm disturbance with a treatment target rather than treating every arrhythmia identically. If abnormal firing reflects altered ion-channel behavior or sympathetic influence, drugs can be selected for their effects on the corresponding currents or autonomic drive. This framework supports treatment decisions involving premature beats, tachyarrhythmias, and other cardiac rhythm disorders.
Studying this process clarifies how nonpacemaking cardiac tissue becomes electrically active under pathological conditions. It supports investigation of drug effects on sodium, calcium, and potassium currents, as well as on sympathetic activity. The resulting knowledge contributes to developing and selecting therapies intended to reduce abnormal impulses and control disorders of cardiac rhythm.