Use of recombinant hirudin to increase the patency rate of microanastomosis in a rabbit model

Microvascular surgical techniques now play an extremely important role in reconstructive surgery. Failures still persist and are most commonly due to thrombotic occlusion of the microvascular anastomosis. Five to 20% of all free tissue transfers and replants are affected. A logical step in the effort to resolve this problem would be the infusion of the newly available recombinant hirudin (r-hirudin). The value of r-hirudin in microvascular surgery has not been investigated. An animal model mimicking the thrombotic mechanisms similar to those in the clinical situation has been described in which a length of rabbit femoral artery is excised, turned inside out and reinserted into the vessel with two standard microvascular anastomoses. The major factors in clinical anastomosis failure are represented in this animal model by medial disruption, imperfect vessel wall alignment, needle holes, trauma, foreign suture material and changes in flow. The type III adventitial collagen turned inward reproduces the clinical problem of adventitial strands becoming caught in the anastomosis. A predictable rate of thrombosis results depending on inversion graft length: a 2 mm segment has an occlusion rate at one week of about 30%. Using this model heparin infusions significantly decrease thrombosis rates compared to saline. Using an almost identical model we have begun a study the effect of r-hirudin on microvascular patency. New Zealand White male rabbits were anaesthetized with ketamine and xylazine. Through a groin incision the femoral vein was catheterized and tubing connected to an infusion pump. The femoral artery was exposed, and the adventitia aggressively removed since it is difficult to minimally debride adventitia in a reproducible fashion.(ABSTRACT TRUNCATED AT 250 WORDS)