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

Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

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 indirectly block calcium...
Antihypertensive Drugs: Types of β-Blockers01:28

Antihypertensive Drugs: Types of β-Blockers

β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and...

You might also read

Related Articles

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

Sort by
Same author

Corrigendum to "When herbal supplements cause heart problems: clinical case report and forensic toxicological" [Toxicol. Rep. 16 (2026) 102239].

Toxicology reports·2026
Same author

Knowledge Assessment on the Management of Acute Cor Pulmonale: An Interdisciplinary Survey Study.

Journal of clinical medicine·2026
Same author

When herbal supplements cause heart problems: Clinical case report and forensic toxicological analysis.

Toxicology reports·2026
Same author

Wingless-related integration site (WNT) signaling is activated during the inflammatory response upon cardiac surgery: A translational study.

Frontiers in cardiovascular medicine·2022
Same author

T-cell recovery and evidence of persistent immune activation 12 months after severe COVID-19.

Allergy·2022
Same author

Autoantibodies in COVID-19 correlate with antiviral humoral responses and distinct immune signatures.

Allergy·2022
Same journal

The authors reply.

Critical care medicine·2026
Same journal

Attracting Emergency Medicine Graduates to Surgical Critical Care Training Programs.

Critical care medicine·2026
Same journal

The authors reply.

Critical care medicine·2026
Same journal

Beyond a Snapshot: Tracking Family Prognostic Expectations in the ICU.

Critical care medicine·2026
Same journal

The authors reply.

Critical care medicine·2026
Same journal

Plasma Levels of Soluble ST2 Reflect Extrapulmonary Organ Dysfunction and Predict Outcomes in Acute Respiratory Failure: Beware of Potential Confounders.

Critical care medicine·2026
See all related articles

Related Experiment Videos

Beta-block the septic heart.

Alain Rudiger1

  • 1Intensive Care Unit, University Hospital Zurich, Zurich, Switzerland. alain.rudiger@usz.ch

Critical Care Medicine
|December 18, 2010
PubMed
Summary
This summary is machine-generated.

Beta-blocker therapy shows promise in treating septic patients by reducing heart rate and preserving cardiac function. Further research is needed to determine optimal dosage and timing for sepsis treatment.

Related Experiment Videos

Area of Science:

  • Cardiology
  • Pharmacology
  • Critical Care Medicine

Background:

  • Sepsis syndrome can cause cardiac depression by attenuating cardiomyocyte adrenergic response.
  • Cardiomyocytes reduce energy expenditure and enter a hibernation-like state during sepsis.
  • Understanding this mechanism is crucial for developing effective sepsis treatments.

Purpose of the Study:

  • To review the efficacy of beta-blocker therapy in managing septic patients.
  • To explore the role of beta-blockers in mitigating cardiac dysfunction during sepsis.

Main Methods:

  • Literature review of studies on beta-blocker therapy in sepsis.
  • Analysis of preclinical (animal) and clinical data.

Main Results:

  • Beta-blockers reduced heart rate and maintained stroke volume in septic animals.
  • Esmolol preserved cardiac function and prevented adrenergic pathway downregulation.
  • Beta-blockers decreased inflammatory response and lung injury in animal models.
  • Metoprolol administration improved blood pressure and cardiac indices in septic shock patients.

Conclusions:

  • Preclinical and clinical studies suggest beta-1 receptor blockers are beneficial in sepsis.
  • Optimal dosage and timing of beta-blocker administration require further investigation.