Date of Award
2011
Degree Type
Thesis
Degree Name
Master of Science in Biomedical Sciences
First Advisor
Lindon Young, PhD
Second Advisor
Ruth C. Borghaei, PhD
Third Advisor
Michael McGuinness, PhD
Fourth Advisor
Marcus Bell, PhD
Abstract
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
Recommended Citation
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.
https://digitalcommons.pcom.edu/biomed/7