Abstract
The pathophysiological mechanisms of heart failure (HF) stems were mainly from longstanding overactivation of the sympathetic nervous system and renin-angiotensin-aldosterone system. Recent studies highlighted the potential benefits of β1-adrenoceptor (β1-AR) blocker combined with β2-adrenergic receptor (β2-AR) agonist in patients with HF. Long-term exposure to fine particulate air pollution, such as particulate matter ≤ 2.5 μm in diameter (PM2.5), has been found associated with acute myocardial infarction (AMI) which is the most common cause of congestive HF. In this study, we have investigated the effect of combined metoprolol and terbutaline on cardiac function in a rat model of AMI exposed to PM2.5. Our results demonstrated that short-term exposure to PM2.5 contributes to aggravate cardiac function in rats with myocardial infarction. The combined use of β1-AR blocker and β2-AR agonist is superior to β1-AR blocker alone for the treatment of AMI rats exposed to PM2.5. The combination of β1-AR blocker and β2-AR agonist may decrease the mortality of patients with myocardial infarction who have been exposed to PM2.5.
Highlights
Introduction βAdrenergic receptor (β-adrenoceptor, β-AR) is an important member of sympathetic nervous system, which plays an important role in regulating the heart function by mediating the physiological effect of catecholamines [1]. β-AR has at least 3 subtypes (β1, β2, and β3), and the former two are important in the regulation of excitation-contraction coupling of myocardium and have positive inotropic response related to cell growth [2]
The aim of this study is to investigate the effect of metoprolol and terbutaline on cardiac function in a rat model of myocardial infarction rats after exposure to PM2.5
Measurements taken from these views revealed left anterior descending (LAD) ligation resulted in cardiac chambers dilatation, wall thinning, and descending myocardial function represented by fractional shortening (%Fractional shortening (FS)) and ejection fraction (%Ejection fraction (EF))
Summary
Introduction βAdrenergic receptor (β-adrenoceptor, β-AR) is an important member of sympathetic nervous system, which plays an important role in regulating the heart function by mediating the physiological effect of catecholamines [1]. β-AR has at least 3 subtypes (β1, β2, and β3), and the former two are important in the regulation of excitation-contraction coupling of myocardium and have positive inotropic response related to cell growth [2]. Adrenergic receptor (β-adrenoceptor, β-AR) is an important member of sympathetic nervous system, which plays an important role in regulating the heart function by mediating the physiological effect of catecholamines [1]. Activation of β1-adrenergic receptor (β1-AR) can induce myocardial cell hypertrophy, apoptosis, cell necrosis, and myocardial remodeling activity in the earlier stage of heart failure. Β2-Adrenergic receptor (β2AR) signalling can grant protection against programmed cell death in myocytes, countering the proapoptotic action of β1-adrenoceptor stimulation via a Gi-mediated process [3,4,5]. Β3-adrenergic receptor (β3-AR) is very rare in human cardiac myocytes, which may appear only in severe heart failure. It has been observed that long-term [11,12,13] or shortterm [14, 15] PM exposures might trigger acute ischemic heart disease. The possible mechanisms include activation of the sympathetic nervous system, oxidative stress, inflammation, BioMed Research International atherosclerosis, and destruction of blood coagulation, affecting the cardiovascular system, for instance, ischemic stroke [16, 17], echocardiography (ECG) ST-segment depression [18, 19], increased plasma viscosity [20], increased circulating markers of inflammation [21, 22], and changes in heart rate variability [23, 24]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
