Broeders M A, Doevendans P A, Maessen J G, van Gorsel E, Egbrink M G, Daemen M J, Tangelder G J, Reneman R S, van der Zee R
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
J Thorac Cardiovasc Surg. 2001 Aug;122(2):305-9. doi: 10.1067/mtc.2001.113602.
Endothelial nitric oxide inhibits smooth muscle cell proliferation, reducing the chance of vascular intimal thickening. In this study we investigated whether the superior long-term patency of the internal thoracic artery in human coronary bypass grafting compared with that of the saphenous vein could be explained by different levels of nitric oxide production.
The baseline endogenous nitric oxide production appeared to be 50% higher in the internal thoracic artery than in the saphenous vein. Previously, it was shown that vascular endothelial growth factor and the vascular endothelial growth factor receptors KDR (Flk-1) and Flt-1 are expressed in both internal thoracic arteries and saphenous veins and that vascular endothelial growth factor receptor density was higher in internal thoracic arteries than in saphenous veins. Therefore, we also investigated the influence of vascular endothelial growth factor on nitric oxide release in both the internal thoracic artery and the saphenous vein.
Vascular endothelial growth factor augmented nitric oxide production by approximately 50% in the saphenous vein and 100% in the internal thoracic artery. As shown by means of immunohistochemistry, expression of endothelial constitutive nitric oxide synthase was similar in the internal thoracic artery and the saphenous vein, and no inducible nitric oxide synthase was expressed in any of the vascular segments.
Vascular endothelial growth factor augments endothelial constitutive nitric oxide synthase-dependent nitric oxide release to a greater extent in the internal thoracic artery than in the saphenous vein. These findings may help to explain the long-term superiority of the internal thoracic artery versus the saphenous vein as a conduit for coronary artery bypass.
内皮型一氧化氮可抑制平滑肌细胞增殖，降低血管内膜增厚的几率。在本研究中，我们探究了在人体冠状动脉搭桥术中，胸廓内动脉较隐静脉具有更高的长期通畅率是否可由一氧化氮产生水平的差异来解释。
胸廓内动脉的基线内源性一氧化氮产生量似乎比隐静脉高50%。此前研究表明，血管内皮生长因子及其血管内皮生长因子受体KDR（Flk-1）和Flt-1在胸廓内动脉和隐静脉中均有表达，且胸廓内动脉中的血管内皮生长因子受体密度高于隐静脉。因此，我们还研究了血管内皮生长因子对胸廓内动脉和隐静脉中一氧化氮释放的影响。
血管内皮生长因子使隐静脉中的一氧化氮产生量增加了约50%，使胸廓内动脉中的一氧化氮产生量增加了100%。免疫组织化学结果显示，胸廓内动脉和隐静脉中内皮型组成型一氧化氮合酶的表达相似，且在任何血管段均未检测到诱导型一氧化氮合酶的表达。
血管内皮生长因子增强内皮型组成型一氧化氮合酶依赖性一氧化氮释放的程度在胸廓内动脉中比在隐静脉中更大。这些发现可能有助于解释胸廓内动脉作为冠状动脉搭桥管道相对于隐静脉的长期优势。
