[Effect of trapidil on prostacyclin formation by rabbit heart tissue]

The release of prostacycline-like compound (PGI2) from the rabbit myocardium was estimated from its ability to inhibit platelet aggregation. Pieces of cardiac tissue were incubated in 0.05% M Tris buffer (pH 8) with arachidonic acid for 10 minutes. The aliquot of incubation medium was added to the rabbit platelet-rich plasma, and PGI2 generation was estimated from the ADP-induced aggregation as compared with antiaggregation activity produced by a known amount of synthetic PGI2. Trapidil (0.7 mM) increased PGI2 generation in the rabbit myocardium from 0.22 +/- 0.03 to 0.41 +/- 0.07 ng/mg wet weight of tissue (n = 7), p less than 0.01), but had no influence on the radioimmunologically assayed content of prostaglandins E and F2 in the incubation medium. Activation effect of trapidil on PGI2 generation in the rat aorta (Kawamura et al, 1980) and rabbit heart (our data), and its inhibitory effect both on the biosynthesis and thromboxan A2 action (Ohnishi et al, 1981) suggest that antiaggregation and coronarolytic actions, positive inotropic and chronotropic effects of trapidil on the myocardium are mediated via local generation of PGI2 and thromboxan A2.