Postoperative abdominal adhesions are more common after gynaecological surgery and appendectomy than after general abdominal surgery (Raf, 1969). They may cause infertility, bowel obstruction and abdominal pain. About 20% of bowel obstructions occur within a year and a further 20% are registered ten years or more after surgery (Menzies and Ellis, 1990). The exact mechanism of adhesion formation is not fully understood. However, adhesions are only formed in the peritoneum when it is damaged by either surgical trauma or inflammatory disease. In a study of rabbits, Elkins et al. (1987) reported that a specific inflammatory reaction occurred in the peritoneum during the 12 h after surgery irrespective of the type of procedure used (excision, abrasion, electrocautery), that is, polymorphonuclear leukocytosis, surface fibrin deposition, white cell exudation, and muscle and mesothelial tissue necrosis. Surface fibrin was not observed 24 h after surgery: the other reactions decreased more slowly. However, the damage caused by electrocautery persisted throughout the 3 week study. Various anti-inflammatory drugs have been used as adjuvant therapies to prevent adhesions without adversely influencing the normal healing process. Swolin (1967a,b) emphasised the importance of high doses of cortisone and Larsson et al. (1977) reported the beneficial effect of oxyphenebutazone in a study on rats. The fibrin matrix appears to play a crucial role in the healing process as well as in the formation of adhesions and the induction of fibroblast activity. Therefore, the use of fibrinolytic activators (plasminogen activators (PA), for example, urokinasetype plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA)) or the inactivation of fibrinolytic inhibitors (plasminogen activator inhibitors (PAI), for example, PAI-1 and PAI-2) as part of the surgical technique could reduce the number of postoperative adhesions. In a study of monkeys, Tisseel