高糖损伤兔主动脉内皮依赖性舒张反应(英文)

目的:研究高糖对兔胸主动脉内皮依赖性舒张反应(EDR)的影响及L-精氨酸、超氧化物歧化酶(SOD)和高糖撤除的作用。方法:以主动脉环EDR为检测指标。结果:高糖可使乙酰胆碱(ACh)诱导的EDR明显受损,高糖撤除24h后不能恢复ACh的舒血管作用,而甘露醇(19.5mmol·L~(-1))不影响血管环EDR。L-精氨酸1mmol·L~(-1)或SOD 150U·L~(-1)可取消高糖对EDR的损伤作用,高糖不影响硝普钠的舒血管作用。结论:高糖可损伤血管EDR,短时间高糖撤除不能逆转,其机制可能与自由基产生及L-精氨酸代谢改变有关。

High glucose impairs endothelium-dependent relaxation in rabbit aorta

AIM: To study the effects of high glucose on endothelium-dependent relaxation (EDR) and the action of L-arginine, 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: 1.6 mumol.L-1 (95% CL: 7.9 nmol.L(-1)-6.3 mumol.L-1) vs normal glucose (5.5 mmol.L-1) EC50: 0.08 mumol.L-1 (95% CL: 0.02 mumol.L(-1)-0.3 mumol.L-1) (P < 0.01), which not reversed followed by a further 24 h incubation in normal glucose M199, EC50: 2.0 mumol.L-1 (95% CL: 0.2 pmol.L(-1)-12.5 mumol.L-1). However, aortic rings incubated with mannitol (19.5 mmol.L-1) relaxed to ACh normally. L-arginine 1 mmol.L-1 or SOD 150 U.L-1 restored ACh relaxation in elevated glucose to normal, EC50: 0.16 mumol.L-1 (95% CL: 0.04 mumol.L(-1)-0.8 mumol.L-1) and 0.16 mumol.L-1 (95% CL: 0.03-0.63 mumol.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.