open access

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

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
DOI: 10.5603/CJ.a2017.0034
·
Pubmed: 28353311
·
Cardiol J 2017;24(4):403-408.

open access

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

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 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.

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 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.

Get Citation

Keywords

cardiac anaphylaxis, isolated perfused rat heart, β-adrenoceptor antagonist, cardiac contractility

About this article
Title

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

Journal

Cardiology Journal

Issue

Vol 24, No 4 (2017)

Pages

403-408

Published online

2017-03-21

DOI

10.5603/CJ.a2017.0034

Pubmed

28353311

Bibliographic record

Cardiol J 2017;24(4):403-408.

Keywords

cardiac anaphylaxis
isolated perfused rat heart
β-adrenoceptor antagonist
cardiac contractility

Authors

Yuhichi Kuda
Toshishige Shibamoto
Wei Yang
Tao Zhang
Mamoru Tanida
Yasutaka Kurata

References (18)
  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.

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk, Poland
tel.:+48 58 320 94 94, fax:+48 58 320 94 60, e-mail: viamedica@viamedica.pl