Abstract 10072: Ischemic Preconditioning Attenuates No-Reflow by Enhancing the Phosphorylation of eNOS at Ser 1179 and Ser 635 via PKA Pathway

Aims: To investigate whether ischemic preconditioning (IPC) protects hearts from myocardial ischemia-reperfusion injury and no-reflow by enhancing the activity of endothelial nitric oxide synthase (eNOS) via protein kinase A (PKA) pathway. Methods and Results: In 90-minute ischemia and 3-hour reperfusion model, Minipigs were randomly assigned to 5 groups: (1) Sham; (2) Control; (3) IPC; (4) IPC+H-89 (1.0μg kg−1 min−1, an inhibitor of PKA); (5) H−89. Compared with control group, IPC significantly decreased the activity of creatine kinase (CK) and myeloperoxidase (MPO) (P<0.05), but H-89 suppressed this effect. The infarct size reduced from 78.5% to 31.3% and 50.4% in IPC and IPC+H-89 group respectively (P<0.05), and the size of no-reflow decreased from 48.6% to 9.7%, 27.3% and 29.5% in IPC, IPC+H-89 and H-89 group respectively (P<0.05). IPC increased the activity of PKA and NOS, and the expression of PKA, Thr 198 p-PKA, Ser1179 p-eNOS and Ser 635 p-eNOS in no-reflow myocardium; while H-89 completely ...