The effect of pentoxifylline on the healing of intestinal anastomosis in rats with experimental obstructive jaundice

Comert M., Taneri F., Tekin E., Ersoy E., Oktemer S., Onuk E., ...More

SURGERY TODAY-THE JAPANESE JOURNAL OF SURGERY, vol.30, no.10, pp.896-902, 2000 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 30 Issue: 10
  • Publication Date: 2000
  • Doi Number: 10.1007/s005950070041
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.896-902
  • Keywords: pentoxifylline, obstructive jaundice, intestinal anastomosis, endotoxemia, tumor necrosis factor alpha, TUMOR-NECROSIS-FACTOR, FACTOR-ALPHA, RENAL-FUNCTION, ENDOTOXIN, CACHECTIN, INTERLEUKIN-1, NEUTROPHILS, CELLS, COMPLICATIONS, SHOCK
  • Dokuz Eylül University Affiliated: No


The aims of this study were (1) to investigate the effect of experimental obstructive jaundice on the healing of intestinal anastomosis, and (2) to investigate the effect of pentoxifylline on the healing of intestinal anastomosis in rats with obstructive jaundice. Obstructive jaundice was induced in rats by the ligation and division of the common bile duct. Four days after this operation, either pentoxifylline or isotonic saline solution was administered intraperitoneally to these jaundiced rats and controls, and then intestinal anastomosis was performed. The concentrations of serum tumor necrosis factor alpha (TNF-alpha) and serum triglyceride of jaundiced and nonjaundiced rats were measured, and the quality of healing was evaluated by measuring the bursting preasure and hydroxyproline content of the anastomoses on the fifth and tenth days of anastomotic healing. Obstructive jaundice resulted in an impaired wound healing of the intestinal anastomosis in the rats. The administration of pentoxifylline to the jaundiced rats resulted in better anastomotic wound healing. The beneficial effects of pentoxifylline on anastomotic healing in rats with obstructive jaundice was attributed to its inhibitor effect on the endotoxin-induced TNF-alpha release from macrophages and monocytes, and the stabilizing effect on the neutrophils.