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1 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA
2 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA
3 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA
4 Department of Biomedical Engineering, Marquette University, Milwaukee, WI, USA
5 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
6 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: jladisa{at}mcw.edu.
Hyperglycemia is associated with generation of reactive oxygen species (ROS), and this action may contribute to accelerated atherogenesis. We tested the hypothesis that hyperglycemia produces alterations in left anterior descending (LAD) coronary artery wall shear stress concomitant with endothelial dysfunction and ROS production in dogs (n=12) instrumented for measurement of LAD blood flow, velocity and diameter. Dogs were randomly assigned to receive vehicle (0.9% saline) or the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (tempol) and were administered intravenous infusions of D-glucose to achieve target blood glucose concentrations of 350 and 600 mg/dl (moderate and severe hyperglycemia, respectively). Endothelial function and ROS generation were assessed by coronary blood flow responses to acetylcholine (10, 30, and 100 ng/kg) and dihydroethidium fluorescence of myocardial biopsies, respectively. Indices of wall shear stress were calculated using conventional fluid dynamics theory. Hyperglycemia produced dose-related endothelial dysfunction, increases in ROS production, and reductions in oscillatory shear stress that were normalized by tempol. The results suggest a direct association between hyperglycemia-induced ROS production, endothelial dysfunction, and decreases in oscillatory shear stress in vivo.
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