The Effects of Direct NADPH Oxidase Inhibitor Apocynin on Real-Time Blood Nitric Oxide and Hydrogen Peroxide Release in Femoral Artery/Vein Ischemia and Reperfusion Injury

Vascular endothelial dysfunction can initiate oxidative stress during ischemialreperfusion (I1R). Endothelial dysfunction is characterized by an increase in blood hydrogen peroxide (H20 2) and a decrease in endothelial-derived nitric oxide (NO) bioavailability. Previous studies using Go 6983, a broad-spectrum protein kinase C inhibitor that can inhibit NADPH oxidase activity, has attenuated blood H20 2 levels during femoral I1R in vivo. This study examines the effects of apocynin (4-hydroxy-3-methoxyacetophenone), a selective NADPH oxidase inhibitor, on real-time blood H20 2 and endothelial-derived NO levels in femoral I1R in vivo. H20 2 or NO micro sensors (100 11m) were inselied into both femoral veins in anesthetized rats. One hind limb was subjected to ischemia by clamping the femoral artery and vein for 20 minutes and allowed to reperfuse for 45 minutes, while the other hind limb served as a sham in the same animal. In the control group, H20 2 was significantly increased by ~ 1-2.5 11M during 45 minutes of reperfusion in the I1R vein when compared to the sham vein (n=7,