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September 1995

Suppressors of Oxygen Metabolites Fail to Reduce Vein Graft Intimal Hyperplasia

Author Affiliations

From the Departments of Surgery (Drs Gates and Hirsch) and Pathology (Dr Karnovsky), Harvard Medical School, Brigham and Women's Hospital (Dr Gates), and Massachusetts General Hospital (Dr Hirsch), Boston.

Arch Surg. 1995;130(9):976-980. doi:10.1001/archsurg.1995.01430090062020

Objective:  To evaluate the role of reactive oxygen metabolites in the initiation of intimal hyperplasia of vein grafts inserted into the arterial circulation.

Setting:  University pathologic research laboratory.

Animals:  Sprague-Dawley rats.

Intervention:  Animals were randomized to receive either the xanthine oxidase inhibitor allopurinol, the iron chelating agent starch-conjugated deferoxamine, or the free-radical scavenger 21-aminosteroid U74389G. Control animals were included for each group. The epigastric vein was inserted into the right common femoral artery. Vein grafts were harvested 30 days postoperatively. The degree of intimal hyperplasia at the two anastomoses as well as at the midgraft was calculated.

Main Outcome Measures:  The vein grafts were divided into three sections designated proximal anastomosis, midgraft, and distal anastomosis. Intimal and medial areas were determined in an observer-blind fashion and expressed as intimal area–medial area ratios.

Results:  Pretreatment of the animals with any of these agents resulted in no significant reduction in the degree of intimal hyperplasia in any treated groups compared with the control animals 30 days postoperatively.

Conclusions:  Arterial reconstruction often involves interposition of vein segments into the arterial circulation. These veins are subject to ischemia and reperfusion, with the potential for generation of reactive oxygen metabolites and subsequent vein graft injury, resulting in intimal hyperplasia. We hypothesized that perioperative pharmacologic intervention either to scavenge or to reduce the production of reactive oxygen metabolites would attenuate the initial vein graft injury and thus limit the subsequent development of intimal hyperplasia. These data create doubt as to the influence of reactive oxygen metabolites in the initiation of intimal hyperplasia in the vein graft.(Arch Surg. 1995;130:976-980)

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