Atrial Tachyarrhythmias Induced by the Combined Effects of β1/2-adrenergic Autoantibodies and Thyroid Hormone in the Rabbit

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• 作者：Hongliang Li (1) (2)
  Benjamin J. Scherlag (1)
  David C. Kem (1) (2)
  Alexandria Benbrook (1)
  Ling Zhang (1)
  Bing Huang (1)
  Madeleine W. Cunningham (3)
  Ralph Lazzara (1)
  Xichun Yu (1) (2) (4)
  
• 关键词：Atrial tachyarrhythmias ; Activating autoantibodies ; β ; adrenergic receptors ; Thyroid hormone ; Rabbit
• 刊名：Journal of Cardiovascular Translational Research
• 出版年：2014
• 出版时间：August 2014
• 年：2014
• 卷：7
• 期：6
• 页码：581-589
• 全文大小：769 KB
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• 作者单位：Hongliang Li (1) (2)
  Benjamin J. Scherlag (1)
  David C. Kem (1) (2)
  Alexandria Benbrook (1)
  Ling Zhang (1)
  Bing Huang (1)
  Madeleine W. Cunningham (3)
  Ralph Lazzara (1)
  Xichun Yu (1) (2) (4)
  
  1. Heart Rhythm Institute, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA
  2. Endocrinology and the Harold Hamm Diabetes Center, Veterans Affairs Medical Center and University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA
  3. Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA
  4. Heart Rhythm Institute and Endocrinology, University of Oklahoma Health Sciences Center, TCH 6E103, 1200 Everett Drive, Oklahoma City, OK, 73104, USA
  
• ISSN：1937-5395

文摘

Activating autoantibodies (AAb) to β-adrenergic receptors (βAR) are associated with atrial fibrillation in patients with Graves-disease. In the present study, we examined the interaction of thyroid hormone with β1/2AR-AAb in inducing atrial tachyarrhythmias in the rabbit. Immunization of rabbits with a β1AR or β2AR second extracellular loop peptide produced high titers of β1AR-AAb or β2AR-AAb. Thyroid hormone in combination with β1AR-AAb or β2AR-AAb induced a significant number of sustained sinus tachycardia and atrial tachycardia, respectively. Both combinations resulted in significantly increased inductions of sustained arrhythmias compared to AAb alone. Thyroid hormone alone induced sustained sinus and junctional tachycardia. Sera from immunized rabbits specifically bound to and activated β1AR or β2AR in transfected cells in vitro. This study demonstrates thyroid hormone qualitatively accentuates the specific arrhythmogenic action of these AAb and quantitatively enhances their rate. Our data support a dual role of AAb and thyroid hormone in Graves-associated tachyarrhythmias.