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The present experiments were conducted to determine whether endothelium-dependent relaxation is impaired in chronic (10-12 wk), streptozotocin-induced diabetic rat aortas and to determine the specificity and sensitivity of diabetic vasculature to oxygen-derived free radicals. Endothelium-dependent relaxation by acetylcholine and ADP was severely impaired in(More)
Nitric oxide release from the endothelium plays an important role in regulation of vascular tone, inhibition of both platelet and leukocyte aggregation and adhesion, and inhibition of cell proliferation. These properties suggest that the level of NO production by the endothelium may play a pivotal role in the regulation of vascular disease. Analysis using(More)
  • G M Pieper
  • 1997
Tetrahydrobiopterin is a cofactor for nitric oxide synthase. In low concentrations of this cofactor, nitric oxide synthase is known to produce less nitric oxide and, correspondingly, enhanced quantities of the oxidant species, hydrogen peroxide. In this study, we tested the hypothesis that an exogenous tetrahydrobiopterin derivative might improve(More)
Long-term diabetes mellitus is characterized by impaired endothelium-dependent relaxation. In contrast, there is limited information on endothelial function in the early stages of the disease. In this study, we evaluated endothelial function ex vivo at early, intermediate and later stages of streptozotocin (STZ)-induced diabetes mellitus. We also evaluated(More)
Defective endothelium-dependent relaxation in diabetic blood vessels may be regulated at the site of synthesis. We tested the hypothesis that acute administration of L-arginine (L-Arg) as substrate for endothelium-derived relaxing factor (EDRF) would normalize defective relaxation to acetylcholine (ACh) in streptozotocin-induced diabetic rat aortic rings.(More)
OBJECTIVE Previous studies suggest a role of superoxide anion radicals (.O2-) in impaired endothelium-dependent relaxation of diabetic blood vessels; however, the role of secondary reactive oxygen species remains unclear. In the present study, we investigated a role of various potential reactive oxygen species in diabetic endothelial dysfunction. METHODS(More)
Brief (15-minute) coronary occlusion and subsequent reperfusion lead to prolonged functional and metabolic abnormalities (stunned myocardium). Previous work suggests that one factor responsible for this phenomenon is oxygen-derived free radicals. The formation of the highly reactive hydroxyl radical requires the presence of metal ions, most importantly(More)
The effects of nicorandil, a nicotinamide nitrate with K(+)-channel-opening activity, was investigated in several models of ischemia-reperfusion injury in conscious and anesthetized dogs or isolated buffer-perfused rat hearts. In several models of reversible ischemic injury (stunned myocardium) in dogs, nicorandil resulted in an enhanced recovery of(More)
The interaction of endothelium-derived relaxing factor (EDRF) and oxygen-derived free radicals may potentially play an important role in the pathophysiology of complications associated with diabetes. In the present study, we investigated spontaneous EDRF release in diabetic rat aorta that is unmasked by the addition of superoxide dismutase (SOD). SOD(More)
The effect of the prostacyclin-mimetic, iloprost, on the reversibly damaged ("stunned") myocardium was studied in barbital-anesthetized, open-chest dogs subjected to 15 minutes of coronary artery occlusion and 3 hours of reperfusion. Regional myocardial segment shortening (%SS) was measured in the subendocardium of nonischemic and ischemic-reperfused areas(More)