Effects of protein kinase C broad spectrum inhibitor Gö 6983 on real-time blood nitric oxide and hydrogen peroxide release in femoral artery/vein ischemia and reperfusion

Background: Vascular endothelial dysfunction is a key component initiating oxidative stress in ischemia/reperfusion (I/R). Endothelial dysfunction is characterized by an increase in hydrogen peroxide (H2O2) and a decrease in the bioavailablity of nitric oxide (NO). Previous studies using protein kinase C (PKC) inhibitor Go 6983 improved cardiac function in myocardial I/R, decreased leukocyte-endothelial interactions and leukocyte superoxide release and increased endothelial-derived NO release in vitro.