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- W3148019062 abstract "AIM: To study the effects of high glucose on endotheli-um-dependent relaxation (EDR) and the action of L-argi-nine, superoxide dismutase (SOD), or glucose re-normalization in aorta. METHODS: Measurement of EDR of the isolated rabbit thoracic aortic rings. RESULTS: Elevated glucose (25 mmol·L-1) caused profound impairment of acetylcholine ( ACh )-induced relaxation, EC50:1.6μmol·L-1(95%CL:7.9μmol·L-1-6.3μmol·L-1) vs normal glucose (5.5 mmol·L-1) 0.08 )μmol·L-1(95 % CL: 0.02μmol·L-1-0.3μmol·L-1) (P0.0l), which not reversed followed by a further 24 h incubation in normal glucose M199, EC50: 2.0μmol·L-1(95 % CL: 0.2 pmol·L-1 - 12.5μmol·L-1). However, aortic rings incubated with mannitol (19.5mmol·L-1) relaxed to ACh normally. L-argi-nine 1 mmol·L-1 or SOD 150 U·L-1 restored ACh relaxation in elevated glucose to normal, EC50: 0.16 μmol·L-1(95 % CL: 0.04μmol·L-1-0.8μmol·L-1) and 0.16μmol·L-1(95%CL:0.03-0.63μmol·L-1). The relaxation in response to sodium nitroprusside was not different between rings exposed to normal or elevated glucose. CONCLUSION: Hyperglycemia impaired EDR, which was not reversible by glucose re-normalization, increased free radical production and altered L-arginine metabolism were involved in this endothelium dysfunction." @default.
- W3148019062 created "2021-04-13" @default.
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- W3148019062 date "2000-01-01" @default.
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- W3148019062 title "High glucose impairs endothelium-dependent relaxation in rabbit aorta" @default.
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