NIkita S Voronkov, Leonid N Maslov, Natalia V Naryzhnaya, Alexander V Mukhomedzyanov
β 1 -AR blockade increases cardiac tolerance to I/R in vivo. β 2 -AR blockade and β 2 - AR stimulation do not affect cardiac resistance to I/R in vivo. β 3 -AR blockade does not affect cardiac resistance to I/R in vivo.
INTRODUCTION: In-hospital mortality in patients with acute myocardial infarction and cardiogenic shock can reach 50%. This is because there are currently no drugs approved for clinical use that can radically reduce infarction size and prevent the development of cardiogenic shock. β- Adrenergic receptor (β-AR) ligands could become such drugs. This article presents a comparative study of the cardioprotective properties of β-AR ligands in ischemia and reperfusion (I/R) of the heart.
METHODS: The study was performed in male Wistar rats. Coronary artery occlusion (CAO, 45 min) and reperfusion (120 min) were carried out in anesthetized animals. Fifteen minutes before CAO the following β-AR ligands were injected intravenously: the selective β 1 -AR antagonist atenolol, β 1 - and β 2 -AR antagonist sotalol, β 1 -, β 2 -, and β 3 -AR antagonist bupranolol, selective β 2 -AR antagonist ICI-118,551, selective β 3 -AR antagonist L- 748,337, and selective β 2 -AR agonist formoterol. It was evaluated the infarct size/area at risk (IS/AAR) ratio.
RESULTS: Sotalol, bupranolol, atenolol, ICI-118,551, and L-748,337 decreased heart rate. Formoterol increased heart rate. Atenolol only reduced the IS/AAR ratio.
CONCLUSION: β 1 -AR blockade increases cardiac tolerance to I/R in vivo. β 2 -AR blockade and β 2 - AR stimulation do not affect cardiac resistance to I/R in vivo. β 3 -AR blockade does not affect cardiac resistance to I/R in vivo.