title: Blockade of β2-adrenoceptor, rather than β1-adrenoceptor, deteriorates cardiac anaphylaxis in isolated blood-perfused rat hearts.
abstract: BACKGROUND
  Cardiac anaphylaxis is one of the features of anaphylactic hypotension. Patients treated with propranolol, a nonselective β-adrenoceptor (AR) antagonist, develop severe anaphylaxis, but the mechanism remains unknown. Under examination were the effects of β1- and β2-AR antagonist on anaphylaxis-induced coronary vasoconstriction and cardiac dysfunction in isolated blood-perfused rat hearts.
  
  
  METHODS
  Isolated hearts from ovalbumin-sensitized Wistar rats were subjected to coronary perfusion with blood at a constant pressure and measurements were made of coronary blood flow and left ventricu-lar (LV) pressure. Following pretreatment with selective β2-AR antagonist ICI118,551 or selective β1-AR antagonist atenolol, cardiac anaphylaxis was induced by intracoronary injections of ovalbumin antigen. LV contractility was evaluated by the maximum increasing rate of systolic LV pressure (dP/dtmax).
  
  
  RESULTS
  In response to antigen administrations, ICI118,551 pretreated hearts showed a greater de-crease in coronary blood flow and consequently a greater increase in coronary vascular resistance than the atenolol pretreated hearts. Pretreatment with ICI118,551 caused a greater decrease in dP/dtmax than those with atenolol.
  
  
  CONCLUSIONS
  Cardiac anaphylaxis-induced contractile dysfunction and coronary spasm are severe in b2-, rather than β1-AR antagonist, pretreated isolated blood-perfused rat hearts.
authors.forename: Yuhichi
authors.initials: Y
authors.lastname: Kuda
authors.affiliation: Kanazawa Medical University. shibamo@kanazawa-med.ac.jp.
authors.forename: Toshishige
authors.initials: T
authors.lastname: Shibamoto
authors.forename: Wei
authors.initials: W
authors.lastname: Yang
authors.forename: Tao
authors.initials: T
authors.lastname: Zhang
authors.forename: Mamoru
authors.initials: M
authors.lastname: Tanida
authors.forename: Yasutaka
authors.initials: Y
authors.lastname: Kurata
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists / Q000633:toxicity*; D058672:Adrenergic beta-2 Receptor Antagonists / Q000633:toxicity*; D000707:Anaphylaxis / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D001262:Atenolol / Q000633:toxicity*; D003329:Coronary Vasospasm / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D003331:Coronary Vessels / Q000187:drug effects* / Q000503:physiopathology; D004195:Disease Models, Animal; D000067268:Isolated Heart Preparation; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D010047:Ovalbumin; D011412:Propanolamines / Q000633:toxicity*; D017208:Rats, Wistar; D018342:Receptors, Adrenergic, beta-1 / Q000187:drug effects / Q000378:metabolism; D018343:Receptors, Adrenergic, beta-2 / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects*; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000187:drug effects*; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: C547789:Adrb1 protein, rat; D058671:Adrenergic beta-1 Receptor Antagonists; D058672:Adrenergic beta-2 Receptor Antagonists; D011412:Propanolamines; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; C026777:ICI 118551; D001262:Atenolol; D010047:Ovalbumin
keywords: cardiac anaphylaxis; cardiac contractility; isolated perfused rat heart; β-adrenoceptor antagonist