lignans and Stomach-Ulcer

Leukotrienes (LT's) are produced in a number of hypersensitivity and in inflammatory conditions in the gastro-intestinal (GI) tract and may contribute to the pathogenesis of GI mucosal injury in their states. LT's do not appear to be produced by the GI mucosa in appreciable quantities under basal "physiological" conditions. Another important leucocyte derived mediator, platelet activating factor (PAF), which is produced in large quantities in hypersensitivity and inflammatory conditions, when given i.v. induces hyperaemia, vascular status and accompanying lesions of the gastric mucosa in rats. This might be related to its hypotensive effects or other actions on the microvasculature of the stomach. Thus PAF may have particular significance in those conditions where there is a profound leucocyte response. It might be an important link between the leucocyte activation that occurs in burn injury and the GI ulceration and haemorrhage that is observed in such patients. There does not appear to be any involvement of PAF in non-inflammatory gastric ulceration induced by aspirin or ethanol+HCl, since the PAF antagonist kadsurenone fails to exert any protective effects when co-administered with either of these drugs.

Topics: Animals; Aspirin; Benzofurans; Ethanol; Gastric Mucosa; Intestinal Mucosa; Lignans; Male; Platelet Activating Factor; Rats; Rats, Inbred Strains; SRS-A; Stomach Ulcer