title: The influence of diabetes on the vasomotor responses of saphenous vein and the development of infra-inguinal vein graft stenosis.
abstract: 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.
authors.affiliation: Department of Surgery, Charing Cross and Westminster Medical School, London, U.K.
authors.forename: R C
authors.initials: RC
authors.lastname: Hicks
authors.forename: J
authors.initials: J
authors.lastname: Moss
authors.forename: D J
authors.initials: DJ
authors.lastname: Higman
authors.forename: R M
authors.initials: RM
authors.lastname: Greenhalgh
authors.forename: J T
authors.initials: JT
authors.lastname: Powell
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000671:Amputation, Surgical; D001807:Blood Vessel Prosthesis; D001920:Bradykinin / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D003094:Collagen / Q000032:analysis; D003922:Diabetes Mellitus, Type 1; D003924:Diabetes Mellitus, Type 2; D003925:Diabetic Angiopathies / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D005340:Fibrinogen / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007511:Ischemia / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery*; D007866:Leg / Q000098:blood supply; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D011183:Postoperative Complications; D012501:Saphenous Vein / Q000473:pathology / Q000503:physiopathology* / Q000648:ultrastructure; D013997:Time Factors; D014652:Vascular Diseases / Q000453:epidemiology* / Q000473:pathology / Q000503:physiopathology; D014656:Vascular Surgical Procedures; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000001:Calcimycin; D005340:Fibrinogen; D003094:Collagen; D001920:Bradykinin; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin