REDUCTION OF ISCHEMIA-REPERFUSION INJURY TO SKIN FLAPS BY MONOCLONAL ANTIBODY TO LEUKOCYTE ENDOTHELIAL ADHESION MOLECULE-1

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  • 虚血再灌流障害皮弁モデルにおける抗LECAM-1抗体の有用性に関する研究
  • キョケツ サイカンリュウ ショウガイ ヒベン モデル ニ オケル コウLECAM 1 コウタイ ノ ユウヨウセイ ニ カンスル ケンキュウ

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Ischemia-reperfusion (I-R) injury continues to be a problem for successful free tissue transfer and replantation after prolonged periods of ischemia. It has been shown that leukocytes and vascular endothelial cells release a variety of inflammatory mediators during reperfusion after ischemia. Leukocyte endothelial adhesion molecule-1 (LECAM-1) is a ligand on the endothelium for some adhesion receptors on leukocytes. The purpose of this study was to evaluate the blockage of leukocyte-endothelial adhesion by a monoclonal antibody (MAb) to LECAM-1 in skin flaps to prevent I-R injury in rats. Male SD rats (225-250 gr) were used. A skin flap (45×30 mm) supplied by the superficial epigastric A&V including the femoral vessels was isolated unilaterally. The femoral vessels were cross-clamped with the epigastric vessels for 9 hours of ischemia. Animals in the treated group received MAb to LECAM -1 i.v. 15 minutes prior to reperfusion; those in the control group received normal saline. Skin flap viability was assessed by tracing the outline of viable and nonviable areas. Data were collected for the following 7 days. These data corroborated with histological evidence on comparable areas of the flap. Tracing analysis revealed an average flap survival area of 89.9+/-24.7% in the treated group and 18.3+/-19.6% in the control group (p<0.005) . Histopathologically, few inflammatory changes could be observed in the treated group, while marked damage was observed in the control group. From this study, we conclud that treating skin flaps with Mab to LECAM -1 was effective for I-R injury after 9 hours of warm ischemia.

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