Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Disturbances in Heart Rhythm01:28

Disturbances in Heart Rhythm

919
Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias.
Arrhythmias are categorized by their speed, rhythm, and origin. A slow...
919
Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

901
Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
901
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

159
Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
159
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

935
Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of...
935
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.3K
Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
1.3K
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

719
Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
719

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Fecal Microbiota Transplant in Parkinson's Disease: Insights into the Gut-Brain Axis and the Challenge of Sustained Response.

Annals of neurology·2026
Same author

Quantitative proteomic profiling of neural cells-specific metabolic reprogramming in response to mitochondrial dysfunction using iMPAQT2.

Mitochondrion·2026
Same author

Active Colitis Attenuates Ventricular Excitation-Contraction Coupling by T-Tubular Remodeling.

Biomolecules·2026
Same author

Prebiotic intervention changes host and microbe proteomes in plasma extracellular vesicles of Parkinson's disease.

Scientific reports·2026
Same author

The Role of Epigenetics in Myocardial Infarction: Mechanism, Biomarkers and Therapeutic Potential.

Galen medical journal·2026
Same author

Systematic health destruction in Iran by Operation Epic Fury.

Lancet (London, England)·2026

Related Experiment Video

Updated: Jun 14, 2025

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples
14:39

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

Published on: April 21, 2014

17.3K

Colitis induced ventricular alternans increases the risk for ventricular arrhythmia.

Carlos H Pereira1, Hiroki Kittaka1, Edward J Ouille V1

  • 1Department of Internal Medicine/Cardiology, Rush University Medical Center, 1750 W. Harrison St., Chicago, IL 60612, USA.

Journal of Molecular and Cellular Cardiology
|May 23, 2025
PubMed
Summary

Inflammatory bowel disease increases arrhythmia risk by altering heart calcium handling via the renin-angiotensin system. Inhibiting this system (ACE or AT1R blockers) may prevent these cardiac changes.

Keywords:
Calcium transient alternansExcitation-contraction couplingInflammatory bowel diseaseRenin-angiotensin systemVentricular alternans

More Related Videos

A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts
07:56

A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts

Published on: February 17, 2023

894
A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis
18:11

A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis

Published on: December 28, 2012

24.2K

Related Experiment Videos

Last Updated: Jun 14, 2025

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples
14:39

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

Published on: April 21, 2014

17.3K
A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts
07:56

A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts

Published on: February 17, 2023

894
A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis
18:11

A Research Method For Detecting Transient Myocardial Ischemia In Patients With Suspected Acute Coronary Syndrome Using Continuous ST-segment Analysis

Published on: December 28, 2012

24.2K

Area of Science:

  • Cardiology
  • Gastroenterology
  • Molecular Biology

Background:

  • Inflammatory bowel disease (IBD) is associated with increased risk of cardiac conduction defects and ventricular arrhythmias.
  • Gut dysbiosis, systemic inflammation, and renin-angiotensin system (RAS) deregulation are linked to IBD and may contribute to cardiac complications.

Purpose of the Study:

  • To investigate the mechanisms by which colitis induces electrophysiological remodeling and increases the risk of ventricular arrhythmia.
  • To explore the role of the renin-angiotensin system in colitis-associated cardiac electrical instability.

Main Methods:

  • A mouse model of dextran sulfate sodium-induced colitis was used to assess cardiac electrophysiology during active inflammation.
  • Electrocardiography, Langendorff-perfused heart electrophysiology (field potential recordings), and isolated ventricular myocyte studies (calcium transient analysis) were performed.
  • The effects of SERCA activator (Istaroxime) and RAS inhibitors (ACE inhibitor, AT1R blocker) were evaluated.

Main Results:

  • Colitis induced prolonged QT duration, increased field potential dispersion, and a higher propensity for ventricular alternans.
  • Isolated myocytes showed increased calcium transient alternans and prolonged duration, linked to attenuated phospholamban phosphorylation.
  • Inhibition of the renin-angiotensin system (ACE or AT1R blockade) prevented the increased alternans inducibility.

Conclusions:

  • Active colitis promotes reversible remodeling of ventricular calcium handling, increasing the risk of arrhythmias like alternans.
  • Renin-angiotensin system activation plays a key role in these colitis-induced cardiac electrophysiological changes.
  • Targeting the RAS may offer a therapeutic benefit for managing cardiac risks in patients with active inflammatory bowel disease.