Increased severity of reperfusion arrhythmias in mouse hearts lacking histamine H3-receptors Academic Article Article uri icon


MeSH Major

  • Cysteine
  • Isoquinolines
  • Neuromuscular Blockade
  • Neuromuscular Nondepolarizing Agents


  • We had previously reported that activation of histamine H(3)-receptors (H(3)R) on cardiac adrenergic nerve terminals decreases norepinephrine (NE) overflow from ischemic hearts and alleviates reperfusion arrhythmias. Thus, we used transgenic mice lacking H(3)R (H(3)R(-/-)) to investigate whether ischemic arrhythmias might be more severe in H(3)R(-/-) hearts than in hearts with intact H(3)R (H(3)R(+/+)). We report a greater incidence and longer duration of ventricular fibrillation (VF) in H(3)R(-/-) hearts subjected to ischemia. VF duration was linearly correlated with NE overflow, suggesting a possible cause-effect relationship between magnitude of NE release and severity of reperfusion arrhythmias. Thus, our findings strengthen a protective antiarrhythmic role of H(3)R in myocardial ischemia. Since malignant tachyarrhythmias cause sudden death in ischemic heart disease, attenuation of NE release by selective H(3)R agonists may represent a new approach in the prevention and treatment of ischemic arrhythmias.

publication date

  • July 4, 2003



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1016/S0006-291X(03)01010-6

PubMed ID

  • 12810089

Additional Document Info

start page

  • 792

end page

  • 6


  • 306


  • 3