Postoperative ileus (POI) is the transient impairment of gastrointestinal motility that develops as a consequence of abdominal surgical procedure. The evidence continues to accumulate indicating that POI is accompanied by a significant increase in patients’ morbidity and by substantial hospitalization costs. The activation of inhibitory spinal and inhibitory sympathetic reflexes, anesthesia, humoral agents, and inflammation have been implicated as causes. Even the gentlest surgical handling of the small intestine sequentially activates an acute inflammatory cascade within the muscle layers of the intestinal wall. Characteristic of this local inflammation is the activation of the macrophages that lie as sentinels within the enteric muscularis. We investigated that the relationship between inflammation in the gut and impaired motility in POI of guinea pig. The colonic motility was significantly impaired in POI compared with control. The degree of inflammation in POI was increased in stomach, small intestine and colon, especially it was significantly higher in colon. Expressions of calprotectin and protease activated receptor-2 (PAR-2) were observed predominantly in colon of POI compared with control. Activation of PAR-2 of colonic epithelial cells may directly affect functional and/or configurational changes of junctional protein and permeability. Therefore, we speculate that the increased permeability of the colon might provide an explanation for delayed resolution of inflammation by exposing the gut to luminal antigen. The increased inflammation and mucosal permeability might play an important role for the postoperative dysmotility. |