Formula diet is a preventive factor in experimentally induced ideal ulcers in rats. A bacteriological study.

We earlier described an experimental model to create recurring chronic ileal inflammation with ulceration in the rat. A 2 cm segment of the distal ileum is excised but left attached to its intact mesentery; the ileum is reanastomosed. The ileal segment will seal off its open ends and a cyst-like structure of varying size will be formed, containing mucus, cell debris and bacteria. Approximately two thirds of the animals develop chronic inflammation with ulceration proximal to the ileal anastomosis. The ileal cyst and the surgical procedure on the distal ileum were shown to be prerequisites of the rat model for the development of lesions. We recently described that, in contrast to rats fed a standard diet, rats fed a hydrolyzed formula diet never developed inflammation or ulceration when subjected to the experimental procedure. In the present study we confirmed these observations and showed that the normal ileal flora (NIF) and the ileal cyst flora (ICF) were significantly influenced by the diets. The bacterial counts of both the aerobic and anaerobic NIF were 2 10log lower, i.e. > or = 99%, in rat fed the formula diet as compared to in those fed standard rat pellets. The NIF of the former group was represented by more aerobic species than the NIF of rats on the standard diet. Compared to the NIF there was a parallel increase in the bacterial counts of the ICF by approximately 2 10log CFU values in both groups of rats. The mean number of anaerobic species, mainly Gram-negative rods of the ICF, increased by approximately 70% in the rats on the standard diet that developed ileal ulceration, whereas identified aerobic species of the ICF decreased by 61% in rats on the formula diet and by 46% in those on the standard diet that did not develop ileal ulceration. The number of anaerobes in those groups of rats remained unchanged. The significant bacteriological differences between the rats that developed ileal ulcers and those which did not indicate that bacteria may be involved, directly or indirectly, in the development of chronic ileal ulceration.

Experimentally induced ileal ulcers in rats. Formula diet is a preventive factor.

We recently described an experimental model in the rat to create recurring chronic ileal inflammation including ulceration. This model is dependent on an "in vivo culture" of normal intestinal contents. In the present experimental study we examined the effect of a polymeric and a hydrolyzed formula diet on the formation of ulcerating lesions using our rat model. Two groups of rats (twenty in each group) were fed either one of these formula diets eight weeks prior to the experimental procedure and this diet was continued until sacrifice eight weeks later. Twenty control rats also underwent the experimental procedure but were fed standard rat pellets for the same time periods. At sacrifice 60% of the control rats had developed ileal ulcers. None of the rats fed the formula diets developed macroscopic ileal inflammation or ulceration. The effectiveness of formula diets in inducing remission in Crohn's disease in humans may be linked to alterations in the intestinal microflora. We hypothesize that the formula diets in this experiment exerted a protective effect against ileal ulceration by altering the ileal microflora. Preliminary studies support this hypothesis but need to be expanded.

Experimentally induced ileal ulcers in rats. A model to study non-specific inflammatory bowel disease.

A surgical technique was used to establish chronic intestinal ulcers in Sprague-Dawley rats. A 2-cm-long segment of the distal ileum was excised and left attached on the mesentery. The ileum was reanastomosed. The excluded ileal segment formed a 'cyst' of various sizes. Initially, the anastomoses healed well, but after 6-8 weeks para-anastomotic ulcers developed in more than 50% of the rats. Histopathology showed a chronic inflammatory reaction with a predominance of mononuclear cells and increased numbers of eosinophilic granulocytes. The surface of the ulcers was covered with bacteria. Penetrating ulcers with fistula formation occurred. It is concluded that this experimental model may be useful for time sequential studies of the development of chronic and ulcerative ileitis. It may also be used to study the effect of medical and surgical regimens for the treatment of non-specific chronic inflammatory bowel disease.

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

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).