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Infarct size limitation by nicorandil

Roles of mitochondrial K_ATP channels, sarcolemmal K_ATP channels, and protein kinase C

^a Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan

View larger version (18K): [in a new window]   Figure 1 Time course of the activation recovery interval (ARI) before and during ischemia. (A) ARIs in control (open circles), nicorandil (solid circles), 5-hydroxydecanoate (5-HD) (open triangles), and 5-HD + nicorandil (solid triangles) groups. (B) ARIs in HMR1098 (open squares) and HMR1098 + nicorandil (solid squares) groups. Open and solid circles are the same as those in A. *p < 0.05 vs. control; #p < 0.05 vs. nicorandil. Base = baseline; Tx = drug treatment.

View larger version (43K): [in a new window]   Figure 2 Effects of calphostin C on translocations of protein kinase C (PKC)- by ischemic preconditioning (PC). The PKC- levels in the cytosol and particulate fraction are expressed as percentages of the total. Ischemic preconditioning significantly reduced PKC- in the cycotol and increased PKC in the particulate fraction, indicating translocation of PKC- from the cytosol to the particulate fraction. In the hearts pretreated with calphostin C (200 nM), translocation of PKC- was not detected. Open bar = cytosol; hatched bar = particulate. *p < 0.05 vs. baseline. n = 4 in each treatment group.