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

Autor: Mamoru Tanida, Yuhichi Kuda, Wei Yang, Tao Zhang, Yasutaka Kurata, Toshishige Shibamoto
Rok vydání: 2017
Předmět:
Male
medicine.medical_specialty
Time Factors
Ovalbumin
Coronary Vasospasm
Propranolol
Ventricular Function
Left

Propanolamines
Contractility
Ventricular Dysfunction
Left

03 medical and health sciences
0302 clinical medicine
Adrenergic beta-2 Receptor Antagonists
Internal medicine
Ventricular Pressure
Animals
Medicine
Rats
Wistar

030223 otorhinolaryngology
Anaphylaxis
business.industry
Antagonist
Isolated Heart Preparation
General Medicine
Blood flow
medicine.disease
Atenolol
Adrenergic beta-1 Receptor Antagonists
Coronary Vessels
Myocardial Contraction
Disease Models
Animal

medicine.anatomical_structure
030228 respiratory system
Vasoconstriction
Cardiology
Vascular resistance
Receptors
Adrenergic
beta-2

Receptors
Adrenergic
beta-1

Cardiology and Cardiovascular Medicine
business
Perfusion
medicine.drug
Zdroj: Cardiology Journal. 24:403-408
ISSN: 1898-018X
1897-5593
DOI: 10.5603/cj.a2017.0034
Popis: 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.
Databáze: OpenAIRE
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