Medical science monitor : international medical journal of experimental and clinical research · 2009
Prevention of myocardial dysfunction by Eplerenon in experimental tachycardiomyopathy.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Cosín-Aguilar Juan, Hernándiz-Martínez Amparo, Aguilar-Llopis Amparo, Portolés-Sanz Manuel, Díez-Gil José Luis
Аннотация
BACKGROUND: High-rate short-duration ventricular pacing induces myocardial hypokinesis that persists once the hemodynamic conditions have been recovered. The aim was to study the factors that determine the persistence of myocardial dysfunction when ventricular tachycardia has ceased and hemodynamic conditions have been restored.
MATERIAL/METHODS: An in vivo experimental pig model was used consisting of a ventricular pacing series (n=10), a ventricular pacing and aldosterone blockade (eplerenon) series (n=6), and a control series without ventricular pacing (n=6). Electrical stimulation was performed from the epicardial base of the left ventricle at a frequency 60% above the basal rate for 2 hours followed by a recovery period of 60 minutes. Cardiac and myocardial function parameters were studied. Plasma levels of aldosterone, renin activity, and glutathione were measured.
RESULTS: Electrically induced tachycardia produced hemodynamic and myocardial changes that persisted after stimulation had ceased, accompanied by an increase in aldosterone and a coronary flow decrease. These changes were not seen when aldosterone activity was blocked by eplerenon. There was a non-significant elevation in glutathione levels.
CONCLUSIONS: These data show that although participation of other neurohormones cannot be ruled out, aldosterone blockade (eplerenon) ameliorates myocardial dysfunction persisting after ventricular tachycardia by preventing coronary endothelial dysfunction.
MATERIAL/METHODS: An in vivo experimental pig model was used consisting of a ventricular pacing series (n=10), a ventricular pacing and aldosterone blockade (eplerenon) series (n=6), and a control series without ventricular pacing (n=6). Electrical stimulation was performed from the epicardial base of the left ventricle at a frequency 60% above the basal rate for 2 hours followed by a recovery period of 60 minutes. Cardiac and myocardial function parameters were studied. Plasma levels of aldosterone, renin activity, and glutathione were measured.
RESULTS: Electrically induced tachycardia produced hemodynamic and myocardial changes that persisted after stimulation had ceased, accompanied by an increase in aldosterone and a coronary flow decrease. These changes were not seen when aldosterone activity was blocked by eplerenon. There was a non-significant elevation in glutathione levels.
CONCLUSIONS: These data show that although participation of other neurohormones cannot be ruled out, aldosterone blockade (eplerenon) ameliorates myocardial dysfunction persisting after ventricular tachycardia by preventing coronary endothelial dysfunction.