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Received for publication September 17, 2004.
Revised December 6, 2004.
Accepted for publication December 6, 2004.
Diabetes is associated with increased risk for complications following coronary bypass grafting surgery (CABG). Augmented superoxide (·O2-) production plays an important role in diabetic complications by causing vascular dysfunction. The potent vasoconstrictor endothelin-1 (ET-1) is also elevated in diabetes and following CABG. However, the effect of ET-1 on ·O2- generation and/or vascular dysfunction in bypass conduits remained unknown. Accordingly, this study investigated basal and ET-1-stimulated ·O2- production in bypass conduits and determined the effect of ·O2- on conduit reactivity. Saphenous vein (SV) specimens were obtained from nondiabetic (n=24) and diabetic (n=24) patients undergoing CABG. Dihydroethidium (DHE) staining and NAD(P)H oxidase activity assays (5,380 ± 940 vs 16,362 ± 2,550 RLU/mg) demonstrated increased basal ·O2- levels in the diabetes group (p<0.05). Plasma ET-1 levels were associated with elevated basal ·O2- levels and treatment of conduits with exogenous ET-1 further increased ·O2- production and augmented vasoconstriction. Furthermore, vascular relaxation was impaired in the diabetic group (75% vs 40%), which was restored by ·O2- scavenger superoxide dismutase (SOD). These findings suggest that ET-1 causes bypass conduits dysfunction via stimulation of ·O2- production in diabetes. Novel therapies that attenuate ·O2- generation in bypass conduits may improve acute and late outcome of CABG in diabetic patients.
Key words:
NADPH oxidase, coronary bypass surgery, endothelin, saphenous vein, superoxide, vascular reactivity
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