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Related Concept Videos

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: 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...
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...
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...

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Related Experiment Video

Updated: May 29, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
11:56

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

High dose ascorbic acid does not reverse central sympathetic overactivity in chronic heart failure.

M E Gomes1, S El Messaoudi, J W M Lenders

  • 1Department of Internal Medicine Department of Cardiology Department of Pharmacology Toxicology, University Medical Center Nijmegen, Nijmegen, The Netherlands.

Journal of Clinical Pharmacy and Therapeutics
|September 16, 2011
PubMed
Summary

Ascorbic acid, an antioxidant, did not reduce sympathetic overactivity in chronic heart failure patients. This study found no significant changes in nerve activity, heart rate variability, or norepinephrine levels after supplementation.

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Related Experiment Videos

Last Updated: May 29, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
11:56

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Published on: April 11, 2014

Surgical Swine Model of Chronic Cardiac Ischemia Treated by Off-Pump Coronary Artery Bypass Graft Surgery
09:12

Surgical Swine Model of Chronic Cardiac Ischemia Treated by Off-Pump Coronary Artery Bypass Graft Surgery

Published on: March 27, 2018

Area of Science:

  • Cardiology
  • Neurology
  • Pharmacology

Background:

  • Increased central sympathetic activity is common in chronic heart failure (CHF).
  • Reactive oxygen species (ROS) in the brain are implicated in mediating this sympathetic overactivity.
  • Ascorbic acid is a known antioxidant and ROS scavenger.

Purpose of the Study:

  • To investigate if ascorbic acid administration can reverse or reduce sympathetic overactivity in CHF patients.
  • To test the hypothesis that antioxidants can mitigate sympathetic dysfunction in heart failure.

Main Methods:

  • A prospective, randomized, placebo-controlled, double-blind, cross-over trial was conducted.
  • 11 CHF patients received ascorbic acid (2 g/day) or placebo for 3 days.
  • Sympathetic activity was assessed via microneurography (MSNA), heart rate variability (HRV), and plasma norepinephrine.

Main Results:

  • Ascorbic acid administration increased plasma vitamin C levels.
  • No significant effect of ascorbic acid was observed on muscle sympathetic nerve activity (MSNA).
  • Heart rate variability and plasma norepinephrine levels remained unchanged.

Conclusions:

  • Short-term ascorbic acid supplementation does not reverse increased sympathetic activity in CHF patients.
  • The tested dosage of ascorbic acid did not impact key markers of sympathetic nervous system activity.
  • Higher oral doses may not be feasible due to potential side effects.