CIC   05421
CENTRO DE INVESTIGACIONES CARDIOVASCULARES "DR. HORACIO EUGENIO CINGOLANI"
Unidad Ejecutora - UE
artículos
Título:
Cardioprotective effects of a non-alcoholic extract of red wine during ischemia and reperfusion in spontaneously hypertensive rats.
Autor/es:
FANTINELLI, JC; MOSCA, SM
Revista:
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
Editorial:
Blackwell Publishing
Referencias:
Año: 2007 vol. 34 p. 166 - 169
ISSN:
0305-1870
Resumen:
1. We recently reported the cardioprotection conferred by a non-alcoholic extract of Cabernet-Sauvignon red wine (RWE) against alterations derived from ischemia and reperfusion in normotensive rats. The objective of the present study was to assess the effects of RWE on ischemia/reperfusion injury in isolated hearts from spontaneously hypertensive rats (SHR). 2. Isovolumic perfused rat hearts were exposed after stabilization to a 20-min global ischemic period followed by 30 min of reperfusion in absence (ischemic control hearts: IC) and presence of RWE infused prior to ischemia and early in reperfusion. In other hearts, LG-nitro-L-arginine methyl ester (L-NAME)-a nitric oxide synthase inhibitor-was administered prior to RWE infusion (L-NAME + RWE). 3.  Left ventricular developed pressure (LVDP), dP/dtmax, and left ventricular end diastolic pressure (LVEDP) were used to assess myocardial function. 4. At the end of reperfusion LVDP decreased to 47 ± 9 % and dP/dtmax to 46 ± 9 % of baseline values in IC. The RWE treatment significantly improved systolic postischemic recovery (LVDP = 85 ± 8 %; dP/dtmax = 83 ± 5 %) and attenuated the increase of LVEDP (23 ± 6 mmHg in RWE vs 53 ± 8 mmHg in IC, P < 0.05).  5. In L-NAME + RWE group, L-NAME completely abolished the systolic and diastolic protection induced by RWE (LVDP = 44 ± 13 %, dP/dtmax = 43 ± 13 %, LVEDP = 60 ± 10 mmHg). 6. These data are the first demonstration that a non-alcoholic extract of Cabernet-Sauvignon red wine protects to the SHR heart from systolic and diastolic alterations induced by ischemia and reperfusion through a NO-dependent mechanism.