Abstract | INTRODUCTION AND OBJECTIVES: Mechanical response to myocardial stretch has been explained by various mechanisms, which include Na(+)/H(+) exchanger activation by autocrine-paracrine system activity. Drug-induced changes were analyzed to investigate the role of these mechanisms in the electrophysiological responses to acute myocardial stretch. METHODS: RESULTS:
EIPA attenuated the increase in the dominant frequency of stretch-induced fibrillation (control=40.4%; losartan=36% [not significant]; BQ-123=46% [not significant]; and EIPA=22% [P<.001]). During stretch, the activation maps were less complex (P<.0001) and the spectral concentration of the arrhythmia was greater (greater regularity) in the EIPA series: control=18 (3%); EIPA = 26 (9%) (P < .02); losartan=18 (5%) (not significant); and BQ-123=18 (4%) (not significant). CONCLUSIONS:
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Authors | Francisco J Chorro, Irene Del Canto, Laia Brines, Luis Such-Miquel, Conrado Calvo, Carlos Soler, Manuel Zarzoso, Isabel Trapero, Álvaro Tormos, Luis Such |
Journal | Revista espanola de cardiologia (English ed.)
(Rev Esp Cardiol (Engl Ed))
Vol. 68
Issue 12
Pg. 1101-10
(Dec 2015)
ISSN: 1885-5857 [Electronic] Spain |
PMID | 25985899
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved. |
Chemical References |
- Angiotensin II Type 1 Receptor Blockers
- Endothelin Receptor Antagonists
- Epithelial Sodium Channel Blockers
- Peptides, Cyclic
- Sodium-Hydrogen Exchangers
- Amiloride
- Losartan
- cyclo(Trp-Asp-Pro-Val-Leu)
- ethylisopropylamiloride
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Topics |
- Amiloride
(analogs & derivatives, pharmacology)
- Angiotensin II Type 1 Receptor Blockers
(pharmacology)
- Animals
- Endothelin Receptor Antagonists
(pharmacology)
- Epithelial Sodium Channel Blockers
(pharmacology)
- Heart
(drug effects, physiology)
- Losartan
(pharmacology)
- Myocardium
- Peptides, Cyclic
(pharmacology)
- Rabbits
- Sodium-Hydrogen Exchangers
(drug effects)
- Stress, Physiological
(physiology)
- Ventricular Fibrillation
(physiopathology)
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