Vol 24, No 4 (2017)
Original articles — Basic science and experimental cardiology
Published online: 2017-03-21

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Blockade of β2-adrenoceptor, rather than β1-adrenoceptor, deteriorates cardiac anaphylaxis in isolated blood-perfused rat hearts

Yuhichi Kuda, Toshishige Shibamoto, Wei Yang, Tao Zhang, Mamoru Tanida, Yasutaka Kurata
Pubmed: 28353311
Cardiol J 2017;24(4):403-408.


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 ventricu­lar (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 de­crease 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.

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  1. Triggiani M, Patella V, Staiano RI, et al. Allergy and the cardiovascular system. Clin Exp Immunol. 2008; 153 Suppl 1: 7–11.
  2. Hirsh SA. Acute allergic reaction with coronary vasospasm. Am Heart J. 1982; 103(5): 928.
  3. Lombardi A, Vandelli R, Cerè E, et al. Silent acute myocardial infarction following a wasp sting. Ital Heart J. 2003; 4(9): 638–641.
  4. Mueller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007; 7(4): 337–341.
  5. Wagdi P, Mehan VK, Bürgi H, et al. Acute myocardial infarction after wasp stings in a patient with normal coronary arteries. Am Heart J. 1994; 128(4): 820–823.
  6. Kounis NG. Kounis syndrome (allergic angina and allergic myocardial infarction): a natural paradigm? Int J Cardiol. 2006; 110(1): 7–14.
  7. Sun S, Weil MH, Tang W, et al. Cardiac anaphylaxis in the Sprague-Dawley rat. J Lab Clin Med. 1992; 120(4): 589–596.
  8. Vleeming W, van Rooij HH, Wemer J, et al. Characterization and modulation of antigen-induced effects in isolated rat heart. J Cardiovasc Pharmacol. 1991; 18(4): 556–565.
  9. Kuda Y, Kurata Y, Wang M, et al. Major contribution of vasospasm-induced coronary blood flow reduction to anaphylactic ventricular dysfunction assessed in isolated blood-perfused rat heart. Cardiol J. 2014; 21(1): 11–17.
  10. Lang DM. Anaphylactoid and anaphylactic reactions. Hazards of beta-blockers. Drug Saf. 1995; 12(5): 299–304.
  11. Mueller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007; 7(4): 337–341.
  12. Zhang W, Shibamoto T, Kuda Y, et al. Pulmonary vasoconstrictive and bronchoconstrictive responses to anaphylaxis are weakened via β2-adrenoceptor activation by endogenous epinephrine in anesthetized rats. Anesthesiology. 2011; 114(3): 614–623.
  13. Shibamoto T, Cui S, Ruan Z, et al. Hepatic venoconstriction is involved in anaphylactic hypotension in rats. Am J Physiol Heart Circ Physiol. 2005; 289(4): H1436–H1441.
  14. Zhang W, Shibamoto T, Kurata Y, et al. Effects of β-adrenoceptor antagonists on anaphylactic hypotension in conscious rats. Eur J Pharmacol. 2011; 650(1): 303–308.
  15. Unwalla HJ, Horvath G, Roth FD, et al. Albuterol modulates its own transepithelial flux via changes in paracellular permeability. Am J Respir Cell Mol Biol. 2012; 46(4): 551–558.
  16. Spindler V, Waschke J. Beta-adrenergic stimulation contributes to maintenance of endothelial barrier functions under baseline conditions. Microcirculation. 2011; 18(2): 118–127.
  17. Hein TW, Zhang C, Wang W, et al. Heterogeneous beta2-adrenoceptor expression and dilation in coronary arterioles across the left ventricular wall. Circulation. 2004; 110(17): 2708–2712.
  18. Watson DC, Sargianou M, Leivaditis V, et al. Beta2-adrenergic activation via administration of atenolol/formoterol combination increases contractility and coronary blood flow in isolated rat hearts. Hellenic J Cardiol. 2013; 54(5): 341–347.