Skip to main navigation Skip to search Skip to main content

Phospholipase-resistant phosphatidylcholine reduces intra-abdominal adhesions induced by bacterial peritonitis

  • M. Snoj
  • , A. Ar'Rajab
  • , B. Ahrén
  • , K. Larsson
  • , S. Bengmark

Research output: Contribution to journalArticlepeer-review

Abstract

The majority of intra-abdominal adhesions develop postoperatively or following peritonitis. We have previously shown that l-phosphatidylcholine reduces postoperative peritoneal adhesions in rats. In the present study, we examined whether adhesion formation after bacterial peritonitis is also reduced by l-phosphatidylcholine or by dl-α-phosphatidylcholine, which is degraded only 50% by phospholipase A2. Peritonitis was induced in the rat by caecal ligation and double puncture; cecotomy was performed 12, 15, or 18h later. Adhesions were assessed blindly by a scoring system 7 days after cecotomy. When cecotomy was scheduled for 18h after caecal ligation and puncture, the 7-day mortality was 90% (n=20). When cecotomy was performed at 12h, no mortality was seen; however, the adhesion score was low (2.3±0.7). When cecotomy was performed 15h after caecal ligation and puncture, the mortality was 25% and the adhesion score was 4.3±0.9. This figure was reduced significantly by intraperitoneal instillation of l-phosphatidylcholine or dl-α-phosphatidylcholine for 3 subsequent days. However, the mortality increased by l-phosphatidylcholine (P<0.01), whereas mortality after dl-α-phosphatidylcholine remained at 30%. We conclude that administration of both l-phosphatidylcholine and dl-α-phosphatidylcholine decrease adhesion formation after bacterial peritonitis.

Original languageEnglish
Pages (from-to)117-122
Number of pages6
JournalResearch in Experimental Medicine
Volume193
Issue number1
DOIs
StatePublished - Dec 1993

Keywords

  • Adhesions
  • Peritonitis
  • Phosphatidylcholine
  • dl-α-phosphatidylcholine didodecyl

Fingerprint

Dive into the research topics of 'Phospholipase-resistant phosphatidylcholine reduces intra-abdominal adhesions induced by bacterial peritonitis'. Together they form a unique fingerprint.

Cite this