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Am J Physiol Heart Circ Physiol 284: H1552-H1559, 2003. First published January 23, 2003; doi:10.1152/ajpheart.01013.2002
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Vol. 284, Issue 5, H1552-H1559, May 2003

Reactive oxygen species modulate coronary wall shear stress and endothelial function during hyperglycemia

Eric R. Gross*,1,2,3, John F. LaDisa Jr.*,1,3, Dorothee Weihrauch1, Lars E. Olson3, Tobias T. Kress1, Douglas A. Hettrick1,3, Paul S. Pagel1,3, David C. Warltier1,2,3,4, and Judy R. Kersten1,2

Departments of 1 Anesthesiology, 4 Medicine (Division of Cardiovascular Diseases) and 2 Pharmacology and Toxicology, Medical College of Wisconsin and Clement J. Zablocki Department of Veterans Affairs Medical Center, Milwaukee 53226; and 3 Department of Biomedical Engineering, Marquette University, Milwaukee, Wisconsin 53233

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 coronary artery (LAD) 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. Indexes of wall shear stress were calculated with 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.

coronary artery disease; diabetes; oscillatory shear stress; oxidant stress

* E. R. Gross and J. F. LaDisa, Jr. contributed equally to this work.




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