CIC   05421
CENTRO DE INVESTIGACIONES CARDIOVASCULARES "DR. HORACIO EUGENIO CINGOLANI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Post-ischemic mitochondrial and myocardial improvement by a non-alcoholic extract of Argentinian red wine in mice.
Autor/es:
CIOCCI PARDO A; SAID M; FANTINELLI JC; MOSCA SM
Reunión:
Congreso; Reunión Anual de la Sociedad Argentina de Fisiología (SAFIS); 2021
Resumen:
Introduction:We previously reported that the treatment of anon-alcoholic extract of Cabernet-Sauvignon red wine (RWE) was able toattenuate the myocardial stunning.Objectives:Toassess the effects of RWE on myocardium and mitochondria submitted to severeischemia leading to irreversible injury. Methods:Isovolumic perfused mice hearts were exposed after stabilization to a30-min global ischemic period (GI) followed by 2 hours of reperfusion (R) inabsence (ischemic control hearts: IC) andpresence of RWE infused prior to ischemia and early during reperfusion. Infarct size (IS) and lactate dehydrogenase (LDH)release were measured. Leftventricular developed pressure (LVDP), left ventricular end diastolic pressure(LVEDP) and -dP/dtmax were used to assess myocardial systolicfunction, diastolic stiffness and myocardial relaxation, respectively.In isolated mitochondria from hearts submitted to 30-min of GI and10 min of R, untreated and treated with RWE, the permeability transition pore (mPTP)resistance to opening Ca2+-mediatedand membrane potential wereassessed. Data are given as means ± SE and the analysis was performed usingrepeated measures of two-way analysis of variance (ANOVA) with Turkey´spost-test for multiple comparisons among groups. A p value <0.05 wasconsidered significant. Results:RWE significantly decreased the IS (23±3% vs 41±4% inIC, n = 8) and LDH level (199±76U/L vs 519±88U/L in IC, n=8). At the end of R, LVDPand -dP/dtmax were 32±6 % and 30 ±4% vs 16±5 % and 11± 4% in IC,respectively, n=8). LVEDP was not modify by RWE. Mitochondria from RWE treatedhearts (n=4) showed a greater mPTP resistance to opening Ca2+-mediatedand a lesser depolarization than untreated hearts mitochondria (n=4). Conclusion:These data demonstratedthat RWE decreased the cell death, reduced the post-ischemic myocardial contractilityand relaxation dysfunction and improved the mitochondrial state at reperfusion.