The objective was to analyze the mechanism of the protection induced by a nonalcoholic extract of red wine (RWE) on ischemia/reperfusion injury. Isovolumic perfused rat hearts were exposed after stabilization to a 20-min global ischemic period followed by 30 min of reperfusion in absence and presence of RWE infused prior to ischemia and early in reperfusion. In other hearts, 5-hydroxydecanoate (5-HD, 100 μM), a selective mitochondrial KATP blocker, chelerythrine (1 μM), a protein kinase C blocker, or LG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, was administered prior to RWE infusion. Left ventricular developed pressure (LVDP), +dP/dtmax, and left ventricular end-diastolic pressure (LVEDP) were used to assess myocardial function. The lactate dehydrogenase release during reperfusion was measured. After the ischemic period, LVDP decreased to 61 ± 4% and +dP/dtmax to 62 ± 5% of baseline values at the end of reperfusion. The infusion of RWE resulted in a complete recovery of systolic function (LVDP = 102 ± 4%; +dP/dtmax = 101 ± 4%) and in an attenuation of the increase of LVEDP (20 ± 3 Hg versus 42 ± 4 mm Hg, p < 0.05). The treatment with RWE did not produce lactate dehydrogenase release during reperfusion. 5-HD and chelerythrine completely abolished the protection induced by RWE (mechanical and enzymatic). L-NAME partially abolished the systolic improvement induced by RWE but returned lactate dehydrogenase loss to ischemic control values. The diastolic protection afforded by RWE was not altered by L-NAME. These data are the first demonstration that mitochondrial KATP channels and nitric oxide are involved in the protection against ischemia/reperfusion conferred by a nonalcoholic RWE.
- K channel
- Nitric oxide
- Red wine
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine