REPERFUSION INJURY IN VASCULARIZED BONE ALLOGRAFTS

Citation
Cg. Moran et al., REPERFUSION INJURY IN VASCULARIZED BONE ALLOGRAFTS, Journal of orthopaedic research, 13(3), 1995, pp. 368-374
Citations number
35
Categorie Soggetti
Orthopedics
ISSN journal
07360266
Volume
13
Issue
3
Year of publication
1995
Pages
368 - 374
Database
ISI
SICI code
0736-0266(1995)13:3<368:RIIVBA>2.0.ZU;2-7
Abstract
A vascularized allograft canine tibia was used to evaluate the preserv ation 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 degrees C) for 20 hours with University of Wisconsin solution. Following stora ge, each pair of bones was transplanted, by microvascular anastomosis, to a recipient dog, and bone blood flow was estimated using the radio labeled microsphere method. Adrenoreceptor control mechanisms were eva luated in one specimen, and endothelial function was evaluated in the contralateral specimen. Alpha(1)-adrenoreceptor blockade produced a si gnificant increase (89 +/- 80%) in bone blood flow (p < 0.05). A furth er increase (99 +/- 56%) was observed with the addition of alpha(2)-bl ockade (p < 0.01). Acetylcholine produced a decrease (65 +/- 65%) in b lood flow (p < 0.1). This effect was inhibited by L-NG-monomethyl-argi nine, which resulted in an increase (53 +/- 47%) in bone blood flow (p < 0.05). The no-reflow phenomenon was observed in two vascularized al lografts. These results demonstrate that smooth muscle adrenoreceptors were preserved successfully for 24 hours. In contrast, endothelial fu nction was abnormal. There was no evidence that the endothelium was pr oducing endothelium-derived relaxing factor, and the results suggest t hat an endothelium-derived constricting factor dependent on L-arginine was produced during reperfusion. It is concluded that University of W isconsin solution does not preserve normal endothelial function in the microcirculation of bone.