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

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