This paper is only available as a PDF. To read, Please Download here.
Abstract
Studies on the prevention of peritoneal adhesions often address the impairment of
adhesion formation by a special drug without any attempts to elucidate the working
principles. In the present study PEG 4000 was compared with dextran 70 with respect
to the influence on adhesion formation, inflammatory reaction, and collagen deposition.
Adhesions were created in 30 rats by standardized crushing of the cecum. The animals
were randomly allocated to 3 experimental groups receiving an intraabdominal instillation
of 5 ml 20% PEG, dextran 70, or 0.9% NaCl. On Day 7 the adhesions were scored; additionally,
the amount of leukocytes in the peritoneal cavity and the incorporation of collagen
into the adhesion strands were determined. Administration of PEG resulted in a significant
reduction of the adhesion score from 10.3 (NaCl) to 2.3, whereas dextran had no effect
(score 11.0). This finding correlated with the leukocyte number which was reduced
by 44% after PEG but was not affected by dextran. The collagen content of the adhesion
strands was significantly decreased by PEG as well as by dextran when compared to
the NaCl controls. In our model PEG was highly effective in the impairment of adhesion
formation. The positive effect was mediated by a reduction of the inflammatory reaction
which resulted in a decreased deposition of collagen into the adhesion strands.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Journal of Surgical ResearchAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
Article info
Identification
Copyright
© 1997 Academic Press. Published by Elsevier Inc. All rights reserved.