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 |
| Externí odkaz: |
|