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Titolo:
Atenolol depresses post-ischaemic recovery in the isolated rat heart
Autore:
Allibardi, S; Merati, G; Chierchia, S; Samaja, M;
Indirizzi:
Univ Milan, Dipartimento Sci & Tecnol Biomed, I-20090 Milan, Italy Univ Milan Milan Italy I-20090 Sci & Tecnol Biomed, I-20090 Milan, Italy Univ Brescia, Cattedra Fisiol, Brescia, Italy Univ Brescia Brescia Italy niv Brescia, Cattedra Fisiol, Brescia, Italy Ist San Raffaele, Milan, Italy Ist San Raffaele Milan ItalyIst San Raffaele, Milan, Italy
Titolo Testata:
PHARMACOLOGICAL RESEARCH
fascicolo: 6, volume: 39, anno: 1999,
pagine: 431 - 435
SICI:
1043-6618(199906)39:6<431:ADPRIT>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCARDIAL-METABOLISM; BETA-BLOCKADE; DISEASE; PROPRANOLOL; BLOCKERS; INJURY;
Keywords:
low-flow ischaemia; beta-blocker; bioenergetics; high-energy phosphates;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Samaja, M UnivItalyn, Dipartimento Sci & Tecnol Biomed, Via Cervi 93, I-20090 Milan, Univ Milan Via Cervi 93 Milan Italy I-20090 93, I-20090 Milan,
Citazione:
S. Allibardi et al., "Atenolol depresses post-ischaemic recovery in the isolated rat heart", PHARMAC RES, 39(6), 1999, pp. 431-435

Abstract

Metabolic events during ischaemia are probably important in determining post-ischaemic myocardial recovery. The aim of this study was to assess the effects of the beta-blocker atenolol and the high energy demand in an ischaemia-reperfusion model free of neurohormonal and vascular factors. We exposed Langendorff-perfused isolated rat hearts to low-flow ischaemia (30 min) and reflow (20 min). Three groups of hearts were used: control hearts (n = Il), hearts that were perfused with 2.5 mu g l(-1) atenolol (n = 9), and hearts electrically paced during ischaemia to distinguish the effect of heart rate from that of the drug (n = 9). The hearts were freeze-clamped at the end of reflow to determine high-energy phosphates and their metabolites. During ischaemia, the pressure-rate product was 2.3 +/- 0.2, 5.2 +/- 1.1, and 3.3 +/- 0.3 mmHg 10(3) min in the control, atenolol and paced hearts, respectively. In addition, the ATP turnover rate, calculated from venous (lactate), oxygen uptake and flow, was higher in atenolol (11.2 +/- 1.7 mu mol min(-1)) and paced (8.1 +/- 0.8 mu mol min(-1)) hearts than in control (6.2 +/- 0.8 mu mol min(-1)). At the end of reflow, the pressure x rate product recovered 75.1 +/- 6.4% of baseline in control vs 54.1 +/- 9.1 and 48.8 +/- 4.4% in atenolol and paced hearts (P < 0.05). In addition, the tissue content of ATP was higher in the control hearts (15.8 +/- 1.0 mu mol g(dw)(-1)) than in atenolol (10.5 +/- 2.6 mu mol g(dw)(-1)) and paced (10.9 +/- 1.3 mu mol g(dw)(-1)) hearts. Thus, by suppressing the protective effects of down-regulation, both atenolol and pacing apparently depress myocardial recoveryin this model. (C) 1999 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/09/20 alle ore 09:48:39