Summary Twenty‐two foals were divided into groups of intestinal distension and intestinal ischaemia as methods to induce peritoneal adhesions. In the first group, the lumen of a segment of distal small intestine was occluded without extramural vascular compromise and distended with lactated Ringer's solution to a constant pressure of 25 cm H2O for 2 h within the abdomen. The ischaemic group underwent 70 mins total vascular occlusion of identical segments of bowel. Serosal biopsies were obtained before and after each experimental procedure and following 60 mins of reperfusion. Similar biopsies were harvested from a control group of foals with no bowel occlusions. The foals were destroyed 10 days after surgery and tissues collected for histological and ultrastructural evaluation. Experimental and control mesothelial surfaces were denuded histologically immediately after experimental occlusions. Serosal oedema and cellular infiltration were observed following reperfusion of the ischaemic segments but were present immediately after 2 h of distension. All foals had developed bowel‐to‐bowel and bowel‐to‐mesentery adhesions of the experimental segments. Control foals under 30 days old exhibited mesenteric contraction and thickening of the isolated segment whereas those older than 30 days had little or no mesenteric thickening or contraction. Histologically, in the experimental segments, fibrous tissue had formed on the outer boundary of the original serosa, and new mesothelial‐like cells were present on the surface of fibrous tissue in some areas. Some serosal fibrosis was also seen in most of the control segments.

Summary Reasons for performing study: Treatments addressing variously theorised pathophysiological mechanisms of small intestinal adhesions have been reported. This study applied those classes of treatments to the most clinically relevant aetiology of post operative adhesions. Hypothesis: Treatments addressing the pathophysiology of ischaemia‐reperfusion induced adhesions would accordingly reduce the incidence of adhesions from this model. Methods: Four classes of treatments were administered for 72 h to 16 foals subjected to complete ischaemia followed by reperfusion to create peritoneal adhesions. These groups were: 1) FPG group ‐ flunixin meglumine (1.1 mg/kg bwt i.v., divided q.i.d.), potassium penicillin G (22,000 iu/kg bwt i.v., q.i.d.) and gentamicin (2.2 mg/kg bwt i.v., t.i.d.); 2) HEP group ‐ heparin (80 iu/kg bwt subcut., b.i.d.); 3) DMSO group ‐ dimethylsulphoxide (DMSO) (20 mg/kg bwt [diluted in 500 ml normal saline] i.v., b.i.d.); and 4) SCMC group ‐ sodium carboxymethylcellulose (500 ml 3% sterile solution intraperitoneally, administered only at the beginning of surgery). Results: Post operative intestinal obstruction did not occur in any foal. After 10 days, necropsy revealed bowel‐to‐bowel adhesions in none of the FPG or DMSO groups, in 2/4 of the SCMC group, in 3/4 of the HEP group and 5/6 foals subjected to the procedure without treatment (UIR group). Conclusions: Inhibition of the inflammation associated with ischaemia and reperfusion in foals treated with FPG or DMSO decreased small intestinal adhesions in foals. Potential relevance: Although anti‐inflammatory therapy was shown to eliminate bowel‐bowel adhesions in this controlled study, it must be remembered that clinical cases are without control. These therapies are advised to improve the result but are unlikely to eliminate the problem.