Sneddon J M, Vane J R
William Harvey Research Institute, Saint Bartholomew's Hospital Medical College, London, United Kingdom.
Proc Natl Acad Sci U S A. 1988 Apr;85(8):2800-4. doi: 10.1073/pnas.85.8.2800.
The adhesion of thrombin-stimulated human blood platelets to either the endothelial surface of intact bovine aorta or cultured bovine aortic endothelial cells was studied to determine the role of endothelium-derived relaxing factor in the regulation of platelet adhesion. Endothelial cells and platelets were pretreated with indomethacin to prevent the formation of prostaglandins. The adhesion of thrombin-stimulated platelets to endothelial cells was reduced by superoxide dismutase and bradykinin. The inhibitory effect of both drugs was abolished by hemoglobin and was absent in strips of bovine aorta where the endothelial cells had been removed by scraping. It is suggested that the effects of bradykinin are mediated by the release of endothelium-derived relaxing factor, which is protected from destruction by superoxide dismutase, and that endothelium-derived relaxing factor contributes to the nonadhesive properties of the vascular endothelium.
研究了凝血酶刺激的人血小板与完整牛主动脉内皮表面或培养的牛主动脉内皮细胞的黏附情况,以确定内皮衍生舒张因子在调节血小板黏附中的作用。内皮细胞和血小板用吲哚美辛预处理以防止前列腺素的形成。超氧化物歧化酶和缓激肽可降低凝血酶刺激的血小板与内皮细胞的黏附。两种药物的抑制作用均被血红蛋白消除,且在通过刮擦去除内皮细胞的牛主动脉条中不存在这种抑制作用。提示缓激肽的作用是由内皮衍生舒张因子的释放介导的,超氧化物歧化酶可保护其免受破坏,且内皮衍生舒张因子有助于血管内皮的非黏附特性。