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Titolo:
Gap junction blockers decrease defibrillation thresholds without changes in ventricular refractoriness in isolated rabbit hearts
Autore:
Qi, XQ; Varma, P; Newman, D; Dorian, P;
Indirizzi:
Univ Toronto, St Michaels Hosp, Dept Med, Toronto, ON M5B 1W8, Canada UnivToronto Toronto ON Canada M5B 1W8 t Med, Toronto, ON M5B 1W8, Canada
Titolo Testata:
CIRCULATION
fascicolo: 13, volume: 104, anno: 2001,
pagine: 1544 - 1549
SICI:
0009-7322(20010925)104:13<1544:GJBDDT>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENERGY-REQUIREMENTS; CARDIAC-CELLS; ANTIARRHYTHMIC DRUGS; IMPULSE PROPAGATION; CANINE MODEL; FIBRILLATION; CONDUCTION; MECHANISM; TACHYCARDIA; RECORDINGS;
Keywords:
defibrillation; blockers; refractoriness; dispersion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Dorian, P Univ Toronto, St Michaels Hosp, Dept Med, 30 Bond St,Room 7-050Q, Toronto,ON M5B 1W8, Canada Univ Toronto 30 Bond St,Room 7-050Q Toronto ONCanada M5B 1W8 da
Citazione:
X.Q. Qi et al., "Gap junction blockers decrease defibrillation thresholds without changes in ventricular refractoriness in isolated rabbit hearts", CIRCULATION, 104(13), 2001, pp. 1544-1549

Abstract

Background-The maintenance and termination of reentry arrhythmias are determined by tissue properties such as refractoriness and conduction velocity. Although the effects of Na+ and K+ channel block on electrophysiological properties and defibrillation threshold (DFT) have been studied, little is known about the effect of gap junction blockers on defibrillation and tissueelectrophysiological properties. Methods and Results-Triplicate DFTs (volts) were obtained before and 15 minutes after 4 mu mol/L 16-doxyl-stearic acid (16-DSA, n=8), 1 mmol/L 1-heptanol (n=12) (both gap junction blockers), 3 mug/mL lidocaine (a sodium channel blocker) (n=8), and respective controls (n=27) in isolated perfused rabbit hearts. DFT decreased after 16-DSA (23 +/- 14%, P <0.01) and 1-heptanol(21 +/- 16%, P <0.01) but increased after lidocaine (26 +/- 28%, P <0.05). Ventricular fibrillation cycle length (VFCL) and QRS duration increased after all 3 agents, by 36 +/- 19% and 44 +/- 16% (16-DSA), 87 +/- 42% and 49 /- 15% (heptanol), and 57 +/- 20% and 43 +/- 26% (lidocaine), respectively(all P <0.01). Spatially averaged temporal VFCL dispersion decreased significantly after all 3 agents, by 47 +/- 42% (16-DSA, P <0.05), 74 +/- 19% (1-heptanol, P <0.01), and 82 +/- 13% (lidocaine, P <0.01), respectively. Ventricular effective refractory period and monophasic action potential duration at 90% repolarization were unchanged after 16-DSA and 1-heptanol (P=NS) but increased after lidocaine (16 +/- 13%, P <0.01, and 6 +/-5%, P=NS, respectively). There were no significant changes in DFT or any other electrophysiological variable in control hearts. Conclusions-Electrical uncoupling by 16-DSA and 1-heptanol significantly lowers DFT and dispersion of VFCL without altering refractoriness; lidocaine, at doses resulting in similar slowing of conduction, increases DFT.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 23:18:14