Free radicals mediate endothelial cell dysfunction caused by elevated glucose

Free radicals mediate endothelial cell dysfunction caused by elevated glucose cell A. COHEN Research, Unit, Robert Dawson Evans Department of Clinical School of Medicine, Boston, Massachusetts 02118 Tesfamariam, Belay, Richard A. Cohen. mediate endothelial cell caused by elevated . Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H321H326, 1992.-Impaired -dependent relaxation occurs in diabetic rabbit aorta normal aorta exposed to elevated concentrations of is prevented by cyclooxygenase inhibitors. The role of in the endothelial cell impairment was examined with radical scavengers in aortas from rabbits fed with probucol (1% wt/wt, a lipidsoluble antioxidant). Rings of aorta suspended for measurement of isometric tension were incubated for 6 h in control (5.5 mM) or elevated (44 mM) . Impairment of dependent relaxation to acetylcholine caused by exposure to elevated was prevented by superoxide dismutase, catalase, deferoxamine, or allopurinol did not occur in aortas from probucol-fed rabbits. Similarly, impairment of acetylcholine relaxations in aortas from alloxan-induced diabetic rabbits was restored to normal by superoxide dismutase. Oxygenderived generated by xanthine oxidase also caused impaired acetylcholine relaxations. Exposure of aortic segments to elevated or to xanthine oxidase caused a significant increase in release of immunoreactive prostanoids. These data indicate that the endothelial cell caused by elevated is mediated by that are likely generated http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Free radicals mediate endothelial cell dysfunction caused by elevated glucose

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Abstract

cell A. COHEN Research, Unit, Robert Dawson Evans Department of Clinical School of Medicine, Boston, Massachusetts 02118 Tesfamariam, Belay, Richard A. Cohen. mediate endothelial cell caused by elevated . Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H321H326, 1992.-Impaired -dependent relaxation occurs in diabetic rabbit aorta normal aorta exposed to elevated concentrations of is prevented by cyclooxygenase inhibitors. The role of in the endothelial cell impairment was examined with radical scavengers in aortas from rabbits fed with probucol (1% wt/wt, a lipidsoluble antioxidant). Rings of aorta suspended for measurement of isometric tension were incubated for 6 h in control (5.5 mM) or elevated (44 mM) . Impairment of dependent relaxation to acetylcholine caused by exposure to elevated was prevented by superoxide dismutase, catalase, deferoxamine, or allopurinol did not occur in aortas from probucol-fed rabbits. Similarly, impairment of acetylcholine relaxations in aortas from alloxan-induced diabetic rabbits was restored to normal by superoxide dismutase. Oxygenderived generated by xanthine oxidase also caused impaired acetylcholine relaxations. Exposure of aortic segments to elevated or to xanthine oxidase caused a significant increase in release of immunoreactive prostanoids. These data indicate that the endothelial cell caused by elevated is mediated by that are likely generated

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Aug 1, 1992

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