We used two experimental models to prove that resveratrol (trans-3,4′,5-trihydroxystilbene) reduces cardiac ischemic-reperfusion injury by means of a nitric oxide- and adenosine-dependent mechanism. (1) Acute ex vivo: resveratrol (10 μM, 10 min) infusion in Langendorff-perfused normoxic rat hearts significantly increased adenosine release and coronary flow compared with baseline. After 30-min low-flow ischemia, vasodilation, still present at reperfusion, was completely abolished by resveratrol plus adenosine antagonist 8-(p-sulfophenyl)theophylline (SPT, 50 μM) administration. (2) Chronic in vivo: rats received tap water containing 25 mg/l resveratrol for 15 days or normal water. Twenty-four hours after, their hearts were Langendorff-perfused and submitted to 60-min low-flow ischemia and reperfusion. The resveratrol-treated hearts showed better functional recovery at reperfusion and significant vasodilation, but no variation in high-energy phosphates ( 31P Nuclear Magnetic Resonance). N G-nitro-L-arginine methyl ester (L-NAME, 30 μM), a nonselective nitric oxide synthase inhibitor, or SPT (50 μM) administered for 10 min prior to the low-flow ischemia cancelled the effects. This suggests that long-term moderate resveratrol consumption could play an important role in late cardioprotective effects.

(Rat), 31P-NMR (nuclear magnetic resonance), Adenosine, Ischemia, low-flow, Preconditioning
dx.doi.org/10.1016/S0014-2999(03)01441-9, hdl.handle.net/1765/64654
European Journal of Pharmacology
Department of Cardiology

Bradamante, S, Barenghi, L, Piccinini, F, Bertelli, A.A.E, de Jonge, R, Beemster, P, & de Jong, J.W. (2003). Resveratrol provides late-phase cardioprotection by means of a nitric oxide- and adenosine-mediated mechanism. European Journal of Pharmacology, 465(1-2), 115–123. doi:10.1016/S0014-2999(03)01441-9