The Impairment of Wound Healing Process is Correlated with Abnormalities of TNF-α Production by Peritoneal Exudate Cells in Obstructive Jaundiced Rats

The wound healing process and production of tumour necrosis factor alpha (TNF-(x) by peritoneal cells of 7-day and 14-day obstructive jaundice (OJ) and sham-operated rats were investigated. In the study the skin wound breaking strength was measured, In addition such histological and biochemical para...

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Veröffentlicht in:HPB Surgery 2000-01, Vol.2000 (5), p.311-318
Hauptverfasser: Dawiskiba, J, Kwiatkowska, D, Zimecki, M, Kornafel, P, Tyran, W, Czapińska, E, Woźniak, Z
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Sprache:eng
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Zusammenfassung:The wound healing process and production of tumour necrosis factor alpha (TNF-(x) by peritoneal cells of 7-day and 14-day obstructive jaundice (OJ) and sham-operated rats were investigated. In the study the skin wound breaking strength was measured, In addition such histological and biochemical parameters as fibroblast and endothelial cell proliferation, inflammatory cell infiltration and hydroxyproline content were evaluated in polyurethane sponge discs implanted subcutaneously into rats. TNF-( production by peritoneal exudate cells (PEC), both spontaneous and lipopolysaccharide (LPS)- induced was determined by a bioassay. In OJ rats the process of both early as well as late phase of healing was impaired. The breaking strength of skin wound was decreased, the fibroblast and endothelial cell proliferation and collagen deposition, as well as hydroxyproline content were diminished. In 7 day OJ the numbers of inflammatory cells in the implants were lowered with a .subsequent slight increase on day 14 of OJ. The spontaneous and LPS induced TNF- (x production by PEC were significantly higher in 7 day OJ as compared with sham-operated controls. On day 14 of OJ the LPS-induced TNF-x level was, in contrast, much lower and did not differ much from the spontaneous TNF-(x production. We conclude that the impairment of wound healing in OJ results from disturbances in functioning of the immune system caused by systemic endotoxaemia.
ISSN:0894-8569
1607-8462
DOI:10.1155/2000/82905