fibrin and Enteritis

Topics: Adult; Aged; Autopsy; Brain; Central Venous Pressure; Colitis; Colon; Enteritis; Female; Fibrin; Heart Ventricles; Hemorrhage; Humans; Kidney; Kidney Glomerulus; Kidney Tubules; Liver; Lung; Male; Middle Aged; Myocardium; Necrosis; Pancreas; Shock; Thrombosis

We investigated the effect of dexamethasone on indomethacin-induced ulceration in the rat.. Groups of four rats received oral indomethacin (15 mg/kg) and the jejunal mucosa was examined 24 h later for mucosal ulceration. Three of the groups received oral dexamethasone (1, 3 and 6 mg/kg) 0.5 h prior to indomethacin, while the fourth received vehicle. Haematological evaluation was performed and ulcers were assessed both histologically and immunohistochemically.. Indomethacin caused multifocal jejunal ulceration that was reduced only by the highest dose of dexamethasone (6 mg/kg). Indomethacin caused a significant fall in the blood haemoglobin concentration that was prevented by dexamethasone at all doses. The ulcers induced by indomethacin alone were deep, punched-out and haemorrhagic while the ulcers arising in rats pre-treated with dexamethasone (all doses) were 'plugged' by a white fibrino-purulent exudate. Histologically, the dexamethasone ulcer exudate was composed of bacteria, fibrin, mucus and a significant increase in the numbers of neutrophils. Dexamethasone alone had no significant pathological effect on the small intestine.. We report the observation that dexamethasone at high doses inhibits indomethacin-induced jejunal ulceration in the rat while at low doses it promotes 'plugging' of ulcers with bacteria, fibrin, mucus and neutrophils that probably reduces haemorrhage from the ulcer base.

Topics: Animals; Dexamethasone; Enteritis; Fibrin; Hematologic Tests; Indomethacin; Intestinal Mucosa; Jejunal Diseases; Male; Mucus; Neutrophils; Rats; Rats, Sprague-Dawley; Ulcer

Topics: Animals; Enteritis; Female; Fibrin; Horse Diseases; Horses; Intestinal Mucosa; Intestine, Small

The significance and frequency of fibrin thrombi (FT), the pathological hallmark of disseminated intravascular coagulation (DIC), in ischemic intestine were analyzed in a retrospective study of the infarcted bowel of patients with occlusive mesenteric ischemia (OMI) and nonocclusive mesenteric ischemia (NOMI). Representative intestinal sections were studied from 10 patients with NOMI of the small and/or large bowel and 12 patients, with OMI of varied etiology. Three patients with inflammatory bowel disease and 1 patient with DIC and bowel necrosis were also studied. Routine hematoxylin and eosin stains for fibrin were prepared for each specimen. The number of FT was quantitated. FT were identified in each of the 10 cases of NOMI; however in only 2 were they prominent. FT were identified in 6 of the 12 cases of OMI and in 4 of these 6 they were a prominent feature. Rare FT were present in the cases of inflammatory bowel disease and did not correlate with the inflammatory process. No FT were present in the intestinal sections of the DIC case. FT are a nonspecific feature of necrosis and can be identified in both occlusive and nonocclusive ischemic bowel disease. Their presence in the intestine of NOMI therefore cannot be used to implicate DIC as the primary cause of this entity.

Topics: Blood Platelets; Disseminated Intravascular Coagulation; Enteritis; Fibrin; Humans; Infarction; Intestinal Diseases; Intestines; Ischemia; Mesenteric Vascular Occlusion; Mesentery; Necrosis; Retrospective Studies; Thrombosis