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Titolo:
INOTROPIC EFFECTS OF ALPHA(1)-ADRENERGIC AGONISTS IN MYOCARDIUM FROM RATS WITH POSTINFARCTION HEART-FAILURE
Autore:
LITWIN SE; VATNER DE; MORGAN JP;
Indirizzi:
BETH ISRAEL HOSP,CHARLES A DANA RES INST,DIV CARDIOVASC,330 BROOKLINEAVE BOSTON MA 02215 BETH ISRAEL HOSP,HARVARD THORNDIKE LAB BOSTON MA 02215 HARVARD UNIV,SCH MED,DEPT INTERNAL MED,DIV CARDIOVASC BOSTON MA 02215 NEW ENGLAND REG PRIMATE RES CTR SOUTHBOROUGH MA 01772
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 5, volume: 38, anno: 1995,
pagine: 1553 - 1563
SICI:
0363-6135(1995)38:5<1553:IEOAAI>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; CARDIOMYOPATHIC SYRIAN-HAMSTER; ALPHA-ADRENERGIC STIMULATION; ACTOMYOSIN MGATPASE ACTIVITY; FAILING HUMAN MYOCARDIUM; CARDIAC MYOCYTES; NONINFARCTED MYOCARDIUM; VENTRICULAR MYOCARDIUM; SARCOPLASMIC-RETICULUM; INOSITOL TRISPHOSPHATE;
Keywords:
ALPHA-ADRENERGIC RECEPTORS; MYOCARDIAL CONTRACTION; CALCIUM; MYOCARDIAL INFARCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
64
Recensione:
Indirizzi per estratti:
Citazione:
S.E. Litwin et al., "INOTROPIC EFFECTS OF ALPHA(1)-ADRENERGIC AGONISTS IN MYOCARDIUM FROM RATS WITH POSTINFARCTION HEART-FAILURE", American journal of physiology. Heart and circulatory physiology, 38(5), 1995, pp. 1553-1563

Abstract

In clinical and experimental heart failure, the inotropic response toP-adrenergic receptor stimulation is depressed. Therefore, non-beta-adrenergic mechanisms may assume increasing importance for summoning inotropic reserve in the failing heart. To test the integrity of the inotropic pathway mediated by alpha(1)-adrenergic receptor stimulation ina model of chronic ischemic heart failure, we administered phenylephrine to noninfarcted left ventricular papillary muscles isolated from sham-operated rats (n = 10) and rats with large (> 40% left ventricularcircumference) anterior myocardial infarctions (n = 9). Isometric force was monitored, and intracellular Ca2+ ( Ca-i(2+)) transients were recorded with the bioluminescent protein aequorin. Compared with muscles from sham-operated rats, contractility of muscles from rats with postinfarction heart failure was depressed at extracellular Ca2+ concentrations between 0.5 and 3.0 mM. Phenylephrine produced comparable dose-dependent increases in developed tension (126 +/- 4 vs. 125 +/- 7% of baseline) and peak rate of tension rise (125 +/- 4 vs. 140 +/- 9% of baseline) in muscles from sham and infarcted rats, respectively. There was no significant change in the time course of the isometric twitch or in the time course or amplitude of the Ca-i(2+) transient after phenylephrine administration in muscles from either group. No evidence of Ca,2+ overload, as defined by spontaneous Ca2+ release, was observed during phenylephrine administration in muscles from normal or failing hearts. The density of alpha(1)-adrenoceptors measured with [H-3]prazosin binding in crude membranes isolated from noninfarcted left ventricular tissue was not different in control and infarcted hearts (48 +/- 5vs. 53 +/- 4 fmol/mg protein). These data indicate that the positive inotropic effect of cy-agonists may be preserved in chronic ischemic heart failure. In both normal and failing myocardium, the inotropic effects of al-adrenergic stimulation occurred with little or no increase in Ca-i(2+) availability and no apparent adverse effects on myocardialrelaxation. Therefore, agents that act by similar mechanisms may havecertain therapeutic advantages over traditional inotropic agents in patients with heart failure.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/07/20 alle ore 22:00:47