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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
Author(s) -
Bartol Kyle D.,
Perkins KerryAnne,
Chen Qian,
Young Lindon H
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.639.4
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 Gö 6983 improved cardiac function in myocardial I/R, decreased leukocyte‐endothelial interactions and leukocyte superoxide release and increased endothelial‐derived NO release in vitro. This study examined the effects of Gö 6983 on real‐time H2O2 and NO release in femoral I/R in vivo. NO or H2O2 microsensors (100 μm) were inserted into both femoral veins in the anesthetized rat. One limb is subjected to I/R in which the femoral artery and vein was clamped for 20 min and released for 45 min and the other served as a sham. H2O2 release significantly increased in the I/R compared to the sham femoral vein in the control group (n=5, P<0.01). NO release showed a trend to decrease in the I/R compared to the sham femoral vein in the control group (n=3). Gö 6983 (7.4 μg/kg) given at the beginning of reperfusion significantly decreased H2O2 (n=7, P<0.05) and increased NO release (n=4, P<0.05) compared to control. Collectively, the data suggest that Gö 6983 attenuates oxidative stress in femoral I/R, which may be due to inhibition of leukocyte/endothelial NADPH oxidase and increasing endothelial‐derived NO release.