To investigate the pathophysiology of ischemic heart disease (IHD), tourniquet ischemia on the upper limb was one and change in platelet aggregation, plasma 6-keto-PGF1 alpha concentrations and plasma thromboxane B2 (TXB2) concentrations were studied. At rest, platelet aggregability and plasma TXB2 concentrations were significantly increased in IHD patients compared with those in normal subjects (p less than 0.001 and p less than 0.001, respectively). In normal subjects, platelet aggregability, plasma 6-keto-PGF1 alpha concentrations and plasma TXB2 concentrations rose significantly during ischemia (p less than 0.05, p less than 0.02 and p less than 0.05, respectively). In addition, plasma 6-keto-PGF1 alpha concentrations were significantly lower in IHD patients than in normal subjects during ischemia (p less than 0.005), though there was no significant change in the level of either group at rest. These results suggest that increase in prostacyclin synthesis in normal subjects during tourniquet ischemia may be a defense mechanism to maintain the balance between prostacyclin and thromboxane A2 (TXA2) and to prevent platelet aggregation induced by the procedure. Increase in platelet aggregation and TXA2 generation in IHD patients at rest indicates a close correlation between IHD and platelet reactivity. Tourniquet ischemia induced a significant increase in prostacyclin generation in normal subjects but not in IHD patients, which suggests the production of prostacyclin was impaired in IHD patients during ischemia. A marked different was obvious in prostacyclin and TXA2 generation between IHD patients and normal subjects, and this difference may play an important role in the pathogenesis of IHD.