Hicks R C, Moss J, Higman D J, Greenhalgh R M, Powell J T
Department of Surgery, Charing Cross and Westminster Medical School, London, U.K.
Diabetes. 1997 Jan;46(1):113-8. doi: 10.2337/diab.46.1.113.
There has been a prejudice that diabetes modulates the function of saphenous vein in a manner that predisposes to bypass graft failure, although most of the evidence accrues from animal studies. We have investigated the effect of diabetes on the vasodilator responses and ultrastructure of saphenous vein harvested from patients undergoing infrainguinal bypass surgery for limb salvage and the development of stenoses within the vein grafts. Of 55 consecutive patients undergoing vein bypass surgery for critical ischemia, 16 (29%) were diabetic: diabetes was not a risk factor for graft stenosis, which occurred in 17 of 56 (30%) grafts. Endothelium-dependent relaxation by nitric oxide pathways stimulated after receptor activation (bradykinin and thrombin) was not different in vein rings from diabetic (n = 12) and nondiabetic patients (n = 12). Prostarioid-mediated vasorelaxation was absent in vein rings from diabetic patients, and the production of 6-keto prostaglandin F(1alpha) (PGF(1alpha)) from diabetic vein was only 66 +/- 27 pg x cm-2 x min-1 compared with 112 +/- 20 pg x cm-2 x min-1 from control vein (P = 0.011). Fibrinogen-mediated vasorelaxation, normally inhibited by K+ channel blockers, was negligible in vein from diabetic patients. No ultrastructural differences were observed between the endothelium of saphenous vein harvested from diabetic and nondiabetic patients. However, diabetes was associated significantly with the presence of spiraled collagen in media. The maintenance of receptor-activated stimulation of nitric oxide pathways and the damping of the response to fibrinogen in saphenous vein endothelium may provide, in part, for the good prognosis of vein graft surgery in diabetic patients: diabetes is not a risk factor for early (12 months) infrainguinal vein graft stenosis.
尽管大多数证据来自动物研究，但一直存在一种偏见，即糖尿病会以某种方式调节大隐静脉的功能，从而易导致旁路移植失败。我们研究了糖尿病对从接受下肢旁路手术以挽救肢体的患者获取的大隐静脉的血管舒张反应和超微结构以及静脉移植物内狭窄形成的影响。在连续55例因严重缺血接受静脉旁路手术的患者中，16例（29%）患有糖尿病：糖尿病不是移植物狭窄的危险因素，56例移植物中有17例（30%）发生了狭窄。受体激活（缓激肽和凝血酶）后通过一氧化氮途径刺激的内皮依赖性舒张在糖尿病患者（n = 12）和非糖尿病患者（n = 12）的静脉环中并无差异。糖尿病患者的静脉环中不存在前列腺素介导的血管舒张，糖尿病静脉产生的6-酮前列腺素F(1α)（PGF(1α)）仅为66±27 pg·cm-2·min-1，而对照静脉为112±20 pg·cm-2·min-1（P = 0.011）。通常被钾通道阻滞剂抑制的纤维蛋白原介导的血管舒张在糖尿病患者的静脉中可忽略不计。在从糖尿病患者和非糖尿病患者获取的大隐静脉内皮之间未观察到超微结构差异。然而，糖尿病与中膜中螺旋状胶原的存在显著相关。大隐静脉内皮中一氧化氮途径受体激活刺激的维持以及对纤维蛋白原反应的减弱可能部分解释了糖尿病患者静脉移植手术的良好预后：糖尿病不是早期（12个月）下肢静脉移植物狭窄的危险因素。
