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Selective beta(1)-blockade improves cardiac bioenergetics and function and decreases neuroendocrine activation in rats during early postinfarct remodeling.
Biochem Biophys Res Commun. 2001 Feb 23; 281(2):491-8.BB

Abstract

In spite of the solid evidence that beta-blockade reduces mortality and morbidity in congestive heart failure (CHF) this therapy continues to be underused in clinical praxis. The reason for this may lie in scarcity of knowledge about the mechanisms of beta-blockade action. The major aim of this study was to investigate in vivo whether selective beta(1)-blockade may improve cardiac energy metabolism in rats with myocardial infarction in early postinfarct remodeling phase. Myocardial infarction (MI) was induced in male Sprague-Dawley rats by ligation of the left coronary artery. Two different groups of rats were studied, rats with MI treated with metoprolol (5 mg/kg/h; n = 9) and rats with MI saline treated (n = 9). The treatment with metoprolol was given by subcutaneously implanted minipumps and was initiated at 3 days postinfarct and during the period of 4 weeks. All rats were investigated with noninvasive methods (31)P magnetic resonance spectroscopy (MRS) and transthoracic echocardiography 3 days after induction of MI and 4 weeks later. Phosphocreatine/ATP ratio was normalized after the treatment with metoprolol while it was 50% lower in the saline group (p < 0.001). In the metoprolol group stroke volume and ejection fraction increased while deceleration time of mitral early filling was longer (all p < 0.05). Left ventricular weight as well as volumes and dimensions were similar between the groups. Plasma levels of noradrenaline (p = 0.058), adrenaline (p < 0.01) and brain natriuretic peptide (p = 0.09) were lower in the metoprolol group. Selective beta(1)-blockade with high dose of metoprolol initiated in the early postinfarct phase improves myocardial energy metabolism and function and prevents overactivation of sympathetic system. The beneficial effect on myocardial bioenergetics may be an important mode of action of beta-blockers which contributes to the clinical benefits of the therapy in CHF.

Authors+Show Affiliations

Wallenberg and Lundberg Laboratories, Sahlgrenska University Hospital, 413 45, Göteborg, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11181074

Citation

Omerovic, E, et al. "Selective Beta(1)-blockade Improves Cardiac Bioenergetics and Function and Decreases Neuroendocrine Activation in Rats During Early Postinfarct Remodeling." Biochemical and Biophysical Research Communications, vol. 281, no. 2, 2001, pp. 491-8.
Omerovic E, Bollano E, Mobini R, et al. Selective beta(1)-blockade improves cardiac bioenergetics and function and decreases neuroendocrine activation in rats during early postinfarct remodeling. Biochem Biophys Res Commun. 2001;281(2):491-8.
Omerovic, E., Bollano, E., Mobini, R., Madhu, B., Kujacic, V., Soussi, B., Hjalmarson, A., & Waagstein, F. (2001). Selective beta(1)-blockade improves cardiac bioenergetics and function and decreases neuroendocrine activation in rats during early postinfarct remodeling. Biochemical and Biophysical Research Communications, 281(2), 491-8.
Omerovic E, et al. Selective Beta(1)-blockade Improves Cardiac Bioenergetics and Function and Decreases Neuroendocrine Activation in Rats During Early Postinfarct Remodeling. Biochem Biophys Res Commun. 2001 Feb 23;281(2):491-8. PubMed PMID: 11181074.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selective beta(1)-blockade improves cardiac bioenergetics and function and decreases neuroendocrine activation in rats during early postinfarct remodeling. AU - Omerovic,E, AU - Bollano,E, AU - Mobini,R, AU - Madhu,B, AU - Kujacic,V, AU - Soussi,B, AU - Hjalmarson,A, AU - Waagstein,F, PY - 2001/2/22/pubmed PY - 2001/4/3/medline PY - 2001/2/22/entrez SP - 491 EP - 8 JF - Biochemical and biophysical research communications JO - Biochem Biophys Res Commun VL - 281 IS - 2 N2 - In spite of the solid evidence that beta-blockade reduces mortality and morbidity in congestive heart failure (CHF) this therapy continues to be underused in clinical praxis. The reason for this may lie in scarcity of knowledge about the mechanisms of beta-blockade action. The major aim of this study was to investigate in vivo whether selective beta(1)-blockade may improve cardiac energy metabolism in rats with myocardial infarction in early postinfarct remodeling phase. Myocardial infarction (MI) was induced in male Sprague-Dawley rats by ligation of the left coronary artery. Two different groups of rats were studied, rats with MI treated with metoprolol (5 mg/kg/h; n = 9) and rats with MI saline treated (n = 9). The treatment with metoprolol was given by subcutaneously implanted minipumps and was initiated at 3 days postinfarct and during the period of 4 weeks. All rats were investigated with noninvasive methods (31)P magnetic resonance spectroscopy (MRS) and transthoracic echocardiography 3 days after induction of MI and 4 weeks later. Phosphocreatine/ATP ratio was normalized after the treatment with metoprolol while it was 50% lower in the saline group (p < 0.001). In the metoprolol group stroke volume and ejection fraction increased while deceleration time of mitral early filling was longer (all p < 0.05). Left ventricular weight as well as volumes and dimensions were similar between the groups. Plasma levels of noradrenaline (p = 0.058), adrenaline (p < 0.01) and brain natriuretic peptide (p = 0.09) were lower in the metoprolol group. Selective beta(1)-blockade with high dose of metoprolol initiated in the early postinfarct phase improves myocardial energy metabolism and function and prevents overactivation of sympathetic system. The beneficial effect on myocardial bioenergetics may be an important mode of action of beta-blockers which contributes to the clinical benefits of the therapy in CHF. SN - 0006-291X UR - https://www.unboundmedicine.com/medline/citation/11181074/Selective_beta_1__blockade_improves_cardiac_bioenergetics_and_function_and_decreases_neuroendocrine_activation_in_rats_during_early_postinfarct_remodeling_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006291X01943360 DB - PRIME DP - Unbound Medicine ER -