Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
CALCIUM-DEPENDENT AND SODIUM-DEPENDENT MODULATION OF STRETCH-INDUCED ARRHYTHMIAS IN ISOLATED CANINE VENTRICLES
Autore:
HANSEN DE; STACY GP; TAYLOR LK; JOBE RL; WANG ZF; DENTON PK; ALEXANDER J;
Indirizzi:
VANDERBILT UNIV,SCH MED,DIV CARDIOL,CC-221S MED CTR N NASHVILLE TN 37232 VANDERBILT UNIV,SCH MED,DEPT BIOMED ENGN NASHVILLE TN 37232
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 5, volume: 37, anno: 1995,
pagine: 1803 - 1813
SICI:
0363-6135(1995)37:5<1803:CASMOS>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED ION CHANNELS; MECHANOELECTRICAL FEEDBACK; ACTION-POTENTIALS; PURKINJE-FIBERS; HEART-FAILURE; MUSCLE; MYOCARDIUM; EXCITATION; TRANSIENT; LENGTH;
Keywords:
LIDOCAINE; STRETCH-ACTIVATED CHANNELS; MECHANOELECTRICAL FEEDBACK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
D.E. Hansen et al., "CALCIUM-DEPENDENT AND SODIUM-DEPENDENT MODULATION OF STRETCH-INDUCED ARRHYTHMIAS IN ISOLATED CANINE VENTRICLES", American journal of physiology. Heart and circulatory physiology, 37(5), 1995, pp. 1803-1813

Abstract

Gadolinium-sensitive stretch-activated channels have been implicated in the process of mechanotransduction signaling of ventricular myocardium. Such channels nonspecifically transport Na+ and Ca2+ in the inward direction. We tested the hypothesis that Na+ and Ca2+ influx are important in the genesis of stretch-induced arrhythmias (SIAs) in an isolated, blood-perfused canine ventricle. To elicit SIAs, left ventricular volume was transiently increased in early diastole using a computerized servo-pump system. Monophasic action potential recordings revealedstretch-induced depolarizations (SIDs) that preceded the arrhythmias. In five ventricles, raising the perfusate Ca2+ concentration from 1 to 3 mM increased ventricular sensitivity to SIAs, manifested by a decrease in the volume change required to precipitate an arrhythmia 50% ofthe time (Delta V-50) from 19.5 +/- 2.7 to 15.2 +/- 1.9 ml (P < 0.05). When the perusate Na+ concentration was decreased from 150 to 90 mM in seven ventricles, Delta V-50 greatly increased (31.1 +/- 14.4 vs. 17.7 +/- 5.3 ml, P < 0.05), and SID amplitude decreased by 47% (P = 0.002). The suppression of SIAs with low extracellular Na+ is unlikely tobe mediated by voltage-gated Na+ channels because lidocaine (5 mg/dl)did not alter SID amplitude. Thus the transsarcolemmal Na+ gradient (and probably that of Ca2+) modulates the amplitude of SIDs, which, in turn, initiate SIAs. These data provide initial evidence that Na+ and Ca2+ help mediate the mechanotransduction processes that underly the genesis of SIAs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 11:19:54