Mechanisms involved in ischaemia, metabolism and stress adaptation 607 hibitor 5-HD at a dose of 5 mg.kg-1 40 min before isc, 5) NaHS+ L-NAME treated with NaHS and the synthase of NO inhibitor L-NAME bolus at a dose of 10 mg.kg-1 on the 19th min of isc and 6) NaHS+ Wortmannin treated with NaHS and the PI3/AKT inhibitor wortmannin at a dose of 60μg kg -1 on the 19th min of isc. The infarct size and the area at risk were estimated (%I/R). In a second series of experiments, we determined the

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... tion of tissue AKT, ERK½, eNOS, GSK3β, STAT3 and phopsholamban (PLB) from Control, NaHS and NaHS+DT-2 groups. Results: NaHS reduced %I/R compared to Control (12.3±3.3% vs 46.4±1.8%, p<0.05), the addition of the DT2 abrogated this benefit (39.8±3.4%), 5-HD and L-NAME did not alter the infarct size reduction (14.1±2.0% and 14.7±2.2% respectively, p=NS vs NaHS) whilst wortmannin reversed it (41.8±1.4%, p=NS vs Control). Phosphorylation of AKT, ERK½, and PLB was higher in NaHS vs Control and NaHS+DT-2 groups with no eNOS and GSK3β activation. STAT-3 activation was higher in NaHS and NaHS+DT-2 vs Control. Conclusion: Exogenous administration of H2S induces pharmacological postconditioning via AKT/PKG/PLB and PKG/ ERK½ activation independently of eNOS, GSK3β, JAK/STAT and mitoKATP activation. P3271 | BENCH Pentraxin-3 and galectin-1 are key mediators of the cardioprotective paracrine effects exerted by fetal mesenchymal stem cells isolated from human placenta