Response of visceral peritoneum to abdominal surgery

Authors

  • Dr M.-L. Ivarsson,

    Corresponding author
    1. Colorectal Unit, Department of Surgery, Sahlgrenska University Hospital/Östra, Göteborg University, S-41685 Göteborg, Sweden
    • Colorectal Unit, Department of Surgery, Sahlgrenska University Hospital/Östra, Göteborg University, S-41685 Göteborg, Sweden
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  • P. Falk,

    1. Colorectal Unit, Department of Surgery, Sahlgrenska University Hospital/Östra, Göteborg University, S-41685 Göteborg, Sweden
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  • L. Holmdahl

    1. Colorectal Unit, Department of Surgery, Sahlgrenska University Hospital/Östra, Göteborg University, S-41685 Göteborg, Sweden
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Abstract

Background:

Postoperative adhesion formation has been associated with a reduced capacity to degrade fibrin within the peritoneal cavity. Peritoneal fibrinolytic capacity has been shown to decrease during the course of a surgical operation. The aim of this study was to investigate whether tissue-type plasminogen activator (tPA), a key fibrinolytic enzyme, is released into the peritoneal cavity during operation.

Methods:

Fluid released from the serosal surface of the small bowel was collected in a plastic bag from 16 patients undergoing surgery. Intraoperative blood samples were also taken from seven patients. Concentrations of the fibrinolytic components tPA and urokinase plasminogen activator (uPA), tPA activity and plasminogen activator inhibitor type 1 (PAI-1) concentration were measured by enzyme-linked immunoabsorbent assay.

Results:

Intraoperative tPA concentrations were significantly raised in the peritoneal fluid collected compared with peripheral blood levels (P = 0·008). This resulted in a significantly higher tPA activity in the fluid compared with blood (P = 0·001). However, neither uPA (P = 0·29) nor PAI-1 (P = 0·84) concentrations differed significantly in fluid compared with blood.

Conclusion:

These data suggest that tPA is rapidly released by the visceral peritoneum during abdominal surgery. The different concentrations in peripheral blood and peritoneum suggest that tPA is released from the peritoneum by an active process, and does not solely derive from leakage of plasma.

Presented in part to the International Congress on Peritoneal Repair and Adhesions (PAX, 5th meeting), Grantham, UK, October 1999, and to the XXXVth European Society for Surgical Research in Malmö, Sweden, June 2000 © 2001 British Journal of Surgery Society Ltd

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