Date of Award
Master of Science in Biomedical Sciences
Lindon Young, PhD
Ruth C. Borghaei, PhD
Michael McGuinness, PhD
Marcus Bell, PhD
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 bioavailability of nitric oxide (NO). Previous studies using protein kinase C (PKC) inhibitor Gö 6983 or PKC Beta (β) II inhibitor improved cardiac function in myocardial I/R, decreased leukocyte-endothelial interactions and leukocyte superoxide (SO) release and increased endothelial-derived NO release in vitro. This study examined the effects of Gö 6983 or PKC β II inhibitor on realtime H2O2 and NO release in femoral vein I/R in vivo. NO or H2O2 microsensors (100 μm diameter) were inserted into both femoral veins in the anesthetized rat. One femoral vein was subjected to I/R, which was induced by clamping the femoral artery and vein for 20 min (ischemia) followed by removing the clamp for 45 min (reperfusion). The other, nonischemic femoral vein served as a sham control in the same animal. H2O2 release significantly increased in the I/R limb compared to the sham limb in the control group by 2-2.8 M during reperfusion (n=7, P
Bartol, Kyle D., "The Effects of Protein Kinase C Inhibitors on Blood Nitric Oxide and Hydrogen Peroxide Release in Ischemia and Reperfusion Injury" (2011). PCOM Biomedical Studies Student Scholarship. 7.