Effect of noradrenaline and isoproterenol on lipopolysaccharide-induced tumor necrosis factor-alpha production in whole blood from patients with chronic heart failure and the role of beta-adrenergic receptors

Am J Cardiol. 2005 Apr 1;95(7):885-9. doi: 10.1016/j.amjcard.2004.12.022.

Abstract

Increased levels of tumor necrosis factor-alpha (TNF-alpha) correlate with poor prognoses in chronic heart failure (CHF). This study demonstrated that noradrenaline and isoproterenol inhibit TNF-alpha production in patients with CHF in ex vivo whole blood in a dose-dependent fashion. The beta-blocker bisoprolol abolishes this effect.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic beta-Antagonists / pharmacology
  • Adult
  • Bisoprolol / pharmacology
  • Cardiovascular Agents / pharmacology*
  • Female
  • Heart Failure / blood
  • Heart Failure / physiopathology*
  • Humans
  • Isoproterenol / pharmacology*
  • Lipopolysaccharides / metabolism
  • Male
  • Norepinephrine / pharmacology*
  • Receptors, Adrenergic, beta / drug effects
  • Receptors, Adrenergic, beta / physiology
  • Tumor Necrosis Factor-alpha / analysis
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / drug effects*

Substances

  • Adrenergic beta-Antagonists
  • Cardiovascular Agents
  • Lipopolysaccharides
  • Receptors, Adrenergic, beta
  • Tumor Necrosis Factor-alpha
  • Isoproterenol
  • Norepinephrine
  • Bisoprolol