Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
LONG-TERM BETA-BLOCKER TREATMENT PREVENTS CHRONIC CREATINE-KINASE ANDLACTATE-DEHYDROGENASE SYSTEM CHANGES IN RAT HEARTS AFTER MYOCARDIAL-INFARCTION
Autore:
LASER A; NEUBAUER S; TIAN R; HU K; GAUDRON P; INGWALL JS; ERTL G;
Indirizzi:
UNIV HEIDELBERG,KLINIKUM MANNHEIM,MED KLIN,THEODOR KUTZER UFER 1-3 D-68135 MANNHEIM GERMANY UNIV HEIDELBERG,KLINIKUM MANNHEIM,MED KLIN D-68135 MANNHEIM GERMANY UNIV WURZBURG W-8700 WURZBURG GERMANY BRIGHAM & WOMENS HOSP BOSTON MA 02115
Titolo Testata:
Journal of the American College of Cardiology
fascicolo: 2, volume: 27, anno: 1996,
pagine: 487 - 493
SICI:
0735-1097(1996)27:2<487:LBTPCC>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
ADRENERGIC-BLOCKADE; DILATED CARDIOMYOPATHY; ENERGY-METABOLISM; FAILURE; PROPRANOLOL; PERFORMANCE; HYPERTROPHY; ENERGETICS; INHIBITION; OVERLOAD;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
A. Laser et al., "LONG-TERM BETA-BLOCKER TREATMENT PREVENTS CHRONIC CREATINE-KINASE ANDLACTATE-DEHYDROGENASE SYSTEM CHANGES IN RAT HEARTS AFTER MYOCARDIAL-INFARCTION", Journal of the American College of Cardiology, 27(2), 1996, pp. 487-493

Abstract

Objectives. We tested the hypothesis that long term betablocker treatment with bisoprolol prevents creatine kinase (CK) and lactate dehydrogenase system changes that occur after chronic myocardial infarction. Background. The mechanism of the beneficial effect of beta blocker therapy is still unclear, Methods. Six groups of rats were studied. Sham operated (sham) and hearts with ligated left anterior descending coronary artery (myocardial infarction) were untreated, treated early (be ginning 30 min after infarction) or treated late (beginning 14 days after infarction), After 8 weeks, hearts were isolated and buffer perfused isovolumetrically. With a left ventricular balloon, mechanical function was recorded at an end diastolic pressure of 10 mm Hg. Biopsy samples of noninfarcted left ventricular tissue were taken. Enzyme activities were measured spectrophotometrically; isoenzymes were separated byagar gel electrophoresis; and total creatine levels were measured with high performance liquid chromatography. Results. The decrease in left ventricular developed pressure in untreated hearts (120 +/- 9 vs. 104 +/- 5 mm Hg [mean +/- SE], p < 0.05, sham vs. myocardial infarction)after myocardial infarction was prevented by early treatment (118 +/-9 vs, 113 +/- 4 mm Hg). Late treatment failed to improve mechanical function. Reduction of CK activity occurring in untreated infarcted hearts (6.4 +/- 0.3 vs. 5.1 +/- 0.3 IU/mg protein, p < 0.05, sham vs, myocardial infarction) was prevented by early beta blocker therapy. The increase in CK isoenzyme BE and MB levels, decrease in mitochondrial CKisoenzyme levels and increase in anaerobic lactate dehydrogenase isoenzyme levels in untreated infarcted hearts did not occur during bisoprolol treatment. The decrease in total creatine levels after myocardialinfarction (74.2 +/- 4.9 vs. 54.9 +/- 3.3 nmol/mg protein, p < 0.05, sham vs. myocardial infarction) was prevented by bisoprolol treatment. Early treatment was more effective than late therapy in preventing CKand lactate dehydrogenase system changes. In addition, in sham hearts, a 40% increase of creatine levels above normal levels was detected. Conclusions. Bisoprolol prevented changes in CK and lactate dehydrogenase systems that occur after myocardial infarction, These observationsmay be related to the beneficial effects of long-term beta-blocker treatment in patients with chronic myocardial infarction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 14:15:04