A correlation between the levels of plasma cortisol, gastric mucosal prostaglandins and the degree of gastric ulceration produced by stress in rats was examined. Four groups of rats were evaluated. Group A, the cold stressed group; group B, their controls; group C, those receiving intraperitoneal indomethacin; and group D, those receiving intraperitoneal saline. Group A developed stress ulcers and their gastric mucosal prostaglandin levels (prostaglandin E2 (PGE2) and prostacyclin levels, as measured by its stable metabolite 6-keto-prostaglandin F1 alpha (6-keto-PGF-1 alpha, but not thromboxane) were significantly reduced when compared with their respective non-stressed controls. The plasma cortisol levels in both group A and B increased slightly in the first hour but there was no statistical difference between the two groups and there was no change at 2, 3 or 4 h of stress. Group C (indomethacin) also developed ulcers and had low gastric mucosal prostaglandin levels when compared with group D (saline). The plasma cortisol levels did not alter in either group C or D. It has been postulated that stress ulcers may involve the depletion of gastric mucosal prostaglandin levels which, in turn, may be a consequence of a higher plasma cortisol level. A decrease in gastric prostaglandins independent of any change of plasma cortisol levels was demonstrated in this study and the mechanism of production of stress gastric ulcers remains obscure.