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Ann Thorac Surg 1995;59:1513-1518
© 1995 The Society of Thoracic Surgeons
Department of Surgery II, Okayama University Medical School, Okayama, Japan
Accepted for publication February 27, 1995.
* Address reprint requests to Dr Umemori, Department of Surgery II, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700, Japan.
We evaluated the effect of urokinase on pulmonary microthrombi formation of the donor lung using a canine cadaver left lung allotransplantation model. Donor animals were sacrificed with an intravenous injection of potassium chloride without heparinization and were divided into three groups. In group 1 (n = 6), cadavers were left at room temperature for 1 hour, and lung retrieval was then performed after flushing the lung block with low potassium—dextran-glucose solution. Donor lungs were stored for 3 hours at 8°C. In group 2 (n = 6), donor lungs were treated as in group 1 except that the cadavers were left at room temperature for 2 hours instead of 1 hour before lung retrieval. In group 3 (n = 6), donor lungs were treated as in group 2 except that high-dose urokinase (120,000 IU) was injected into the main pulmonary artery after flushing with low-potassium—dextrose-glucose solution. In all groups after left lung transplantation, the right pulmonary artery was ligated, and recipient animals were followed up for 6 hours after reperfusion. The fibrin degradation product level in the donor lung tissue was also measured. All recipient animals in group 1 survived the 6-hour observation period with excellent gas exchange and stable hemodynamics. Group 3 had significantly better gas exchange than group 2 and similar cardiopulmonary function as group 1. The fibrin degradation product level in the donor lungs before transplantation was significantly higher in group 3 than in group 2. This study supports the theory that urokinase improves lung function after cadaver lung transplantation by fibrinolytic action on pulmonary microthrombi formation in the cadaver donor lungs.
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