The significance of platelet-vessel wall prostaglandin equilibrium during exercise-induced stress.

Alterations in platelet-generated thromboxane A2 (TXA2) and vessel wall-generated prostacyclin (PGI2) have been associated with myocardial ischemia. To examine TXA2-PGI2 equilibrium at rest and during exercise stress, we studied 13 normal subjects and 15 coronary artery disease patients. Plasma TXB2 and 6-keto-PGF1 alpha were measured as stable metabolites of TXA2 and PGI2, respectively, by radioimmunoassay. In normal subjects, plasma TXB2 levels increased 24% during exercise from 135 +/- 30 to 168 +/- 42 pg/ml (p = NS). Plasma 6-keto-PGF1 alpha levels increased 224% from 54 +/- 17 to 175 +/- 57 pg/ml (p less than 0.05). In coronary artery disease patients, although resting plasma TXB2 levels (mean 136 +/- 43 pg/ml) were comparable to levels in normal subjects, a greater increase (82%) occurred during exercise (mean 248 +/- 70 pg/ml; p less than 0.02 compared to resting levels). Resting plasma 6-keto-PGF1 alpha levels (mean 94 +/- 28 pg/ml) were also similar to normal subjects but increased only by 43% during exercise (mean 134 +/- 53 pg/ml; p = NS compared to resting levels). These data suggest that: in normal subjects TXA2 and PGI2 increase during exercise, PGI2 increasing more than TXA2, and although coronary disease patients have resting TXA2 and PGI2 levels in the normal range, TXA2 levels increase more than PGI2 levels during exercise. These observations may have a bearing on the mechanism of exercise-induced angina pectoris in certain coronary artery disease patients.