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J Vasc Surg. 2014 Jul;60(1):202-11. doi: 10.1016/j.jvs.2013.06.004. Epub 2013 Jul 30.

Surgical vein graft preparation promotes cellular dysfunction, oxidative stress, and intimal hyperplasia in human saphenous vein.

Author information

1
Department of Surgery, Vanderbilt University Medical Center, Nashville, Tenn. Electronic address: michael.j.osgood@vanderbilt.edu.
2
Department of Surgery, Vanderbilt University Medical Center, Nashville, Tenn.
3
Department of Surgery, General Hospital of Jinan Military District, Jinan Military District, China.
4
Department of Surgery, Vanderbilt University Medical Center, Nashville, Tenn; Department of Surgery, Tennessee Valley Veterans Affairs Medical Center, Nashville, Tenn.

Abstract

INTRODUCTION:

Human saphenous vein (HSV) is the most widely used bypass conduit for peripheral and coronary vascular reconstructions. However, outcomes are limited by a high rate of intimal hyperplasia (IH). HSV undergoes a series of ex vivo surgical manipulations prior to implantation, including hydrostatic distension, marking, and warm ischemia in solution. We investigated the impact of surgical preparation on HSV cellular function and development of IH in organ culture. We hypothesized that oxidative stress is a mediator of HSV dysfunction.

METHODS:

HSV was collected from patients undergoing vascular bypass before and after surgical preparation. Smooth muscle and endothelial function were measured using a muscle bath. Endothelial preservation was assessed with immunohistochemical staining. An organ culture model was used to investigate the influence of surgical preparation injury on the development of IH. Superoxide levels were measured using a high-performance liquid chromatography-based assay. The influence of oxidative stress on HSV physiologic responses was investigated by exposing HSV to hydrogen peroxide (H2O2).

RESULTS:

Surgical vein graft preparation resulted in smooth muscle and endothelial dysfunction, endothelial denudation, diminished endothelial nitric oxide synthase staining, development of increased IH, and increased levels of reactive oxygen species. Experimental induction of oxidative stress in unmanipulated HSV by treatment with H2O2 promoted endothelial dysfunction. Duration of storage time in solution did not contribute to smooth muscle or endothelial dysfunction.

CONCLUSIONS:

Surgical vein graft preparation causes dysfunction of the smooth muscle and endothelium, endothelial denudation, reduced endothelial nitric oxide synthase expression, and promotes IH in organ culture. Moreover, increased levels of reactive oxygen species are produced and may promote further vein graft dysfunction. These results argue for less injurious means of preparing HSV prior to autologous transplantation into the arterial circulation.

PMID:
23911244
PMCID:
PMC3926896
DOI:
10.1016/j.jvs.2013.06.004
[Indexed for MEDLINE]
Free PMC Article

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