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Titolo:
Enhanced in vivo and in vitro contractile responses to beta(2)-adrenergic receptor stimulation in dogs susceptible to lethal arrhythmias
Autore:
Houle, MS; Altschuld, RA; Billman, GE;
Indirizzi:
Ohio State Univ, Dept Physiol & Cell Biol, Columbus, OH 43210 USA Ohio State Univ Columbus OH USA 43210 & Cell Biol, Columbus, OH 43210 USA Ohio State Univ, Dept Mol & Cellular Biochem, Columbus, OH 43210 USA Ohio State Univ Columbus OH USA 43210 lar Biochem, Columbus, OH 43210 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 4, volume: 91, anno: 2001,
pagine: 1627 - 1637
SICI:
8750-7587(200110)91:4<1627:EIVAIV>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
SUDDEN CARDIAC DEATH; HUMAN VENTRICULAR MYOCARDIUM; DOWN-REGULATION; HEART-FAILURE; IN-VIVO; MYOCYTES; FIBRILLATION; CANINE; CELLS; INFARCTION;
Keywords:
sudden cardiac death; beta-adrenergic receptors; myocardial ischemia; inotropy; contractility; ventricular fibrillation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Billman, GE Ohio State Univ, Dept Physiol & Cell Biol, 302 Hamilton Hall,1645 Neil Ave, Columbus, OH 43210 USA Ohio State Univ 302 Hamilton Hall,1645Neil Ave Columbus OH USA 43210
Citazione:
M.S. Houle et al., "Enhanced in vivo and in vitro contractile responses to beta(2)-adrenergic receptor stimulation in dogs susceptible to lethal arrhythmias", J APP PHYSL, 91(4), 2001, pp. 1627-1637

Abstract

The response to beta -adrenergic receptor (beta -AR) stimulation was evaluated in both isolated cardiomyocytes (video edge detection) and the intact animal (echocardiography) in dogs either susceptible (S) or resistant (R) to ventricular fibrillation induced by a 2-min coronary occlusion during thelast minute of exercise. In the intact animal, velocity of circumferentialfiber shortening (Vcf) was evaluated both before (n = 27, S = 12 and R = 15) and after myocardial infarction. Before infarction, increasing doses of isoproterenol provoked similar contractile and heart rate responses in eachgroup of dogs. Either beta (1)-AR (bisoprolol) or beta (2)-AR (ICI-118551)antagonists reduced the isoproterenol response, with a larger reduction noted after the beta (1)-AR blockade. In contrast, after infarction, isoproterenol induced a significantly larger Vcf and heart rate response in the susceptible animals that was eliminated by beta (2)-AR blockade. The single-cell isotonic shortening response to isoproterenol (100 nM) was also larger in cells obtained from susceptible compared with resistant dogs and was reduced to a greater extent by beta (2)-AR blockade in the susceptible dog myocytes (S, - 48%, n = 6; R, - 15%, n = 9). When considered together, these data suggest that myocardial infarction provoked an enhanced beta (2)-AR response in susceptible, but not resistant, animals.

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Documento generato il 27/01/20 alle ore 16:56:35