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. 2012 Feb 29;32(6):1035–1045. doi: 10.1038/jcbfm.2012.14

Figure 4.

Figure 4

Influence of superoxide and peroxynitrite on reactivity changes and endothelial dysfunction in middle cerebral arteries (MCA) perfused with hyperglycemic MCA occlusion (HG MCAO) plasma. (A) Active lumen diameter versus pressure of nonischemic MCA perfused with physiologic saline solution (PSS) (No plasma), HG MCAO plasma (pl) or HG MCAO plasma+100 μmol/L apocynin. Apocynin did not prevent the decrease in lumen diameter induced by HG MCAO plasma. (B) Active lumen diameter versus pressure of nonischemic MCA perfused with PSS (No plasma), HG MCAO plasma (pl), or HG MCAO plasma+50 μmol/L FeTMPyP. FeTMPyP completely reversed the decrease in lumen diameter induced by HG MCAO plasma. (C) Graph showing percent tone of nonischemic MCA perfused with PSS (No plasma), HG MCAO plasma (pl), HG MCAO plasma+100 μmol/L apocynin, or HG MCAO plasma+50 μmol/L FeTMPyP. Apocynin had little effect on myogenic tone; however, FeTMPyP prevented the increase in tone in response to HG MCAO plasma. (D) Graph showing percent tone in response to 0.1 mmol/L L-NNA under the same experimental conditions described in panel C. Neither apocynin nor FeTMPyP restored the response to L-NNA to No plasma levels, suggesting that the effect of FeTMPyP on decreasing tone in response to HG MCAO plasma may due to inhibiting vasoconstricting properties of peroxynitrite. *P<0.05 versus No plasma; **P<0.01 versus No plasma and ^P<0.05 versus HG MCAO plasma. L-NNA, NOS inhibitor nitro-L-arginine.