Reperfusion injury in vascularized bone allografts

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Abstract
A vascularized allograft canine tibia was used to evaluate the preservation of the osseous microcirculation. Six pairs of adult tibiae were harvested, and a vascular washout was performed with mannitol solution. The bones then were perfused continuously (0.03 ml/min at 5°C) for 20 hours with University of Wisconsin solution. Following storage, each pair of bones was transplanted, by microvasacular anastomosis, to a recipient dog, and bone blood flow was estimated using the radiolabeled microsphere method. Adreno-receptor control mechanisms were evaluated in one specimen, and endothelial function was evaluated in the contralateral specimen. Alpha1-adrenoreceptor blockade produced a significant increase (89 ± 80%) in bone blood flow (p < 0.05). A further increase (99 ± 56%) was observed with the addition of alpha2-blockade (p < 0.01). Acetylcholine produced a decrease (65 ± 65%) in blo od flow (p < 0.1). This effect was inhibited by L-NG-monomethyl-arginine, which resulted in an increase (53 ± 47%) in bone blood flow (p < 0.05). The no-reflow phenomenon was observed in two vascularized allografts. These results demonstrate that smooth muscle adrenoreceptors were preserved successfully for 24 hours. In contrast, endothelial function was abnormal. There was no evidence that the endothelium was producing endothelium-derived relaxing factor, and the results suggest that an endothelium-derived constricting factor dependent on L-arginine was produced during reperfusion. It is concluded that University of Wisconsin solution does not preserve normal endothelial function in the microcirculation of bone.