The role of feces, necrotic tissue, and various blocking agents in the prevention of adhesions

Abstract

Ischemic tissue and intraperitoneal bacteria have been ascribed an etiologic role in the production of intra-abdominal adhesions. To further elucidate the role of these stimuli and to evaluate the potential protective effect of various agents, peritonitis was induced in 160 Sprague-Dawley rats. The experiment was stratified into those animals with peritonitis plus necrotic tissue, solid feces, both, or neither. The agents tested were a nonsteroidal anti-inflammatory (ibuprofen), free radical scavenger (SOD), and an anticoagulant (heparin). Death was less likely to occur in animals treated with heparin (3 of 40 vs. 12 of 40, p less than 0.01) or SOD (4 of 40 vs. 12 of 40, p less than 0.05). Ibuprofen did not increase survival in this model. Heparin protected against adhesions in animals with an ischemic ileum of limb and without solid feces. In animals with a nonischemic isolated segment of ileum and solid feces, adhesion formation was increased in both the ibuprofen and the heparin treatment groups (p less than 0.05).