Effects of propranolol on β- Adrenergic receptor of experimental acute myocardial infarction in rats

Abstract

By using receptor autoradiography to observe the distribution and density of receptors, the effects of propranolol, a β-blocker, on β-adrenergic receptor of experimental acute myocardial infarction (AMI) were studied. One week after ligation of proximate left anterior descend (LAD) coronary artery, [³H] DHA binding sites were markedly decreased in both infarctregion and non-infarct region. After treatment of propranolol (100 μg/kg), the [³H] DHA binding sites were obviously increased in the infarct region, and they were further decreased in the non-infarct region. The ratio of [³H] DHA binding sites of the infarct region to non-infarct region was from 0. 24 at LAD ligation to 0. 87 after propranolol treatment, which was close to 0. 97 of control group (sham operation). The results indicated that the propranolol acted directly on myocardial β- adrenergic through the receptor regulation of the balance of β-receptors between the infarct region and non-infarct region, and improvement of the myocardial consonation and contraction synergism, thereby protecting the heart affected by AMI.

Keywords

acute myocardial infarction / propranolol / β-adrenergic receptor / autoradiography

References

[1] MarokoP R, KfekshusJ K, SobelB E. Factors influencing infarct size following experimental coronary occlusion. Circulation, 1971, 43: 67-67

[2] ReimerK A, RasmussehM M, JenningsR B. Reduction by propranolol of myocardial necrosis following temporary artery occlusion in dogs. Circ Res, 1973, 33: 353-353

[3] Beta Blocker Attack Trial Research Group. A randomized trial of propranolol in patients with acute myocardial infarction. JAMA, 1982, 247: 1701-1701

[4] Beta Blocker Attack Trial Research Group. A ramdomized trial of propranolol in patients with acute myocardial infarction. JAMA, 1983, 250: 2814-2814

[5] RobertD R, WillianE B, RichardJ G, et al. . Effects of propranolol on myocardial infarct size with and without coronary reperfusion in the dog. Cardiov Res, 1981, 15: 411-411

[6] RobertoF, AnnalisaZ. β-Blockers in chronic treatment after acute myocardial infarction. J Cardiovasc, 1989, 14(9): S68-S68

[7] AkeH, GunnarO. Myocardial infarction: Effects of β-Blocker. Circulation, 1991, 84(VI): VI-VI

[8] HeldPH, YusufS. Effects of Beta-blockers and calcium channel blockers in acute myocardial infarction. Eur Heart J, 1993, 14(F): 18-18

[9] FerneresJ, CambouJ B, RuidavelsJ B, et al. . Trends in acute myocardial infarction prognosis and treatment in Southwestern France between 1985 and 1990 (The MONICA Project-Toulous). Am J Cardiol, 1995, 75: 1202-1202

[10] KarlsbergR P, PenkoskeP A, CryesPE, et al. . Rapid activation of the sympathetic nervous system following coronary artery occlusion: relationship to infarct size, site, and haemodynamic impact. Cardiovasc Res, 1979, 13: 523-523

[11] BarryL. Neuroendocrine activation in acute myocardial infarction. Am J Cardiol, 1990, 65: 32-32

[12] CarlJ P. New concepts in pathophysiology of acute myocardial infarction. Am J Cardiol, 1989, 64(4): 2B-2B

[13] MaiselA S, MotulskyH J, InselP A, et al. . External ligation of β-adrenergic receptors promoted by myocardial ischemia. Science, 1985, 230: 183-183