Chester A H, O'Neil G S, Moncada S, Tadjkarimi S, Yacoub M H
National Heart and Lung Institute, Harefield Hospital, Middlesex, UK.
Lancet. 1990 Oct 13;336(8720):897-900. doi: 10.1016/0140-6736(90)92269-n.
Endothelium-dependent relaxations in response to substance P and bradykinin were lower in atherosclerotic than in normal human coronary arteries. The relaxation induced by substance P was inhibited by L-NG-monomethylarginine (L-NMMA), which shows that release of nitric oxide is involved in the mediation of endothelium-dependent relaxation in these arteries. L-NMMA also inhibited a basal component of endothelium-dependent relaxation. The basal secretion of nitric oxide was significantly lower in diseased than in normal arteries. These findings suggest that atherosclerotic human coronary arteries lack an important protective mechanism that normally guards against vasospasm and thrombosis.
与正常人类冠状动脉相比，动脉粥样硬化患者的冠状动脉对P物质和缓激肽的内皮依赖性舒张作用较弱。L-NG-单甲基精氨酸（L-NMMA）抑制了P物质诱导的舒张，这表明一氧化氮的释放参与了这些动脉内皮依赖性舒张的介导过程。L-NMMA还抑制了内皮依赖性舒张的基础成分。患病动脉中一氧化氮的基础分泌显著低于正常动脉。这些发现表明，动脉粥样硬化的人类冠状动脉缺乏一种正常情况下可预防血管痉挛和血栓形成的重要保护机制。
