摘要
用离体兔胸主动脉淋浴式灌注方法探讨左旋精氨酸对内、外源性OFR损伤血管内皮功能的保护作用,结果:用二乙二硫氨基甲酸盐(DETC)产生的内源性OFR与电解缓冲液产生的外源性OFR均可明显抑制血管内皮依赖性扩张,并使血管壁MDA含量增加,左旋精氨酸能对抗内、外源性OFR所致MDA增加与内皮依赖舒血管功能损害。
This study was to investigate the protective effect of l-arginine, a precursor of endothelium-derived relaxing factor (EDRF), against damages due to endogenous or exogenous oxygen free radicals (C)FR) on the aortic endothelium. The superfusion cascade bio-assay of rabbit thoracic aorta was used. Endogenous OFR were generated by di-ethyldithiocarbamate (DETC) to deplete the cytosolic Zn-Cu form of superoxide dismutase (SOD). Exogenous OFR were generated by electrolysis of Krebs' solution. Acetylcholine (ACh) was infused through the donor aortic segment and relaxation of detector aortic ring was used as an indicator of the release of EDRF. The content of malondialdehyde (MDA) in the donor aorta was assayed biochemically. Both DETC and electrolysis inhibited vasodilator responses to ACh and increased MDA content in the aortic segment. Inhibition of DETC was abolished by exogenous SOD.l-Arginine improved impairment of endothelium-dependent relaxation and reduced elevation of MDA content by DETC or electrolysis. These results suggest that l-arginine presents a protective effect of endothelium against damage due to endogenous or exogenous OFR, and that the protective effect of l-arginine may be correlated with reduction in lipid peroxidation.
出处
《中国药理学报》
CSCD
1994年第2期119-123,共5页
Acta Pharmacologica Sinica
基金
Project supported by a Grant from State Education Commission of China.
关键词
左旋精氨酸
自由基
胸主动脉
arginine
diethyldithiocarba- mate
nitric oxide
electrolysis
gen species
thoracic aorta