The Journal of Bone and Joint Surgery, Vol 69, Issue 3 442-449, Copyright © 1987 by Journal of Bone and Joint Surgery, Inc
The use of urokinase in ischemic replanted extremities in rats
TA Zdeblick, JW Shaffer and GA Field
We compared the efficacy of intra-arterial infusion of urokinase, a
fibrinolytic agent, with that of intra-arterial infusion of nitrendipine, a
peripheral calcium-channel blocking agent, in preventing the no-reflow
phenomenon in rats after prolonged ischemia at room temperature. Urokinase
increased the survival of the limbs after both four and five hours of
ischemia at room temperature to 100 per cent compared with 50 and 20 per
cent, respectively, in untreated controls. Nitrendipine significantly
increased the blood flow but failed to significantly increase the survival
of the limb. Scanning electron microscopy was used to assist in the
evaluation of the endothelium of the vessels. The etiological mechanism of
the no-reflow phenomenon appears to be that ischemia damages the
endothelial cells, causing impairment of the fibrinolytic system,
retraction of the endothelial membrane, exposure of the subintimal
collagen, and fibrin-platelet deposition. Thrombosis of the vessels ensues,
resulting in the no-reflow phenomenon. Clinical Relevance: Experimentally,
intra-arterial infusion of urokinase increased the survival of the limb in
replanted extremities that were subjected to ischemia. This effectively
lengthened the safe limit of ischemia at room temperature before
microsurgical replantation or elective free-tissue transfer. Clinical
trials of the use of intra-arterial fibrinolytic agents for the treatment
of revascularized tissue are indicated.
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