EFFECTS OF ISCHEMIC PRECONDITIONING (IP) ON MNSOD CYTOSOLIC ACTIVITY IN HEARTS FROM SHR: ROLE OF NO AND MITOCHONDRIAL KATP CHANNELS

FANTINELLI JC; PÉREZ NUÑEZ I; SCHINELLA GR; MOSCA SM

La Plata, Argentina

Congreso; XXVII Congreso Nacional de Cardiología e ISHR: XCII Reunión Sección Latinoamericana.; 2009

ISHR

Manganese superoxide dismutase (MnSOD) is primarily a mitochondrial enzyme that appears in the cytosol when mitochondrial permeability increases. Our objective was to study the effects of IP on MnSOD cytosolic activity (MnSODc)and infarct size (IS) in hearts isolated from spontaneously hypertensive rats (SHR), a the end of the following protocols: 1) 35min of global ischemia (GI) and 2hs of reperfusion (R); 2) 50min of GI and 2 hs of R; 3) IP1: one cycle of GI 5min-R 10 min previous to GI35; 4) IP3: three cycle of IG 2min-R 5min previous to GI50. To examine the participation of nitric oxide (NO) and mitochondrial KATP channels (mitoKATP) both protocols of IP were repeated in presence of L-NAME (inhibitor of NOsintase) and 5-HD (blockade of mitoKATP). IP1 and IP3 decreased MnSODc [1.8 ± 0.5 and 1.4 ± 0.6 vs 4.8 ± 1.1 and 4.7 ± 0.7 %inh/mgprot for GI35 and GI50, respectively, p<0.05] and IS [IP1: 12 ± 3% vs 35 ± 5 % (IG35); IP3: 22 ± 4 % vs 56 ± 5% (IG50)]. L-NAME and 5-HD treatments abolished the beneficial effects of IP1 and IP3. These data show that IP through NO and mitoKATP reduces MnSOD release into the cytosol and the irreversible injury after IG-R and suggests that an attenuation of mitochondrial permeability would be the mechanism involved in the IP-mediated protection.