The release of prostacyclin (PGI2) by pentoxifylline from human vascular tissue.

The influence of pentoxifylline (Trental) on prostacyclin (PGI2) formation was studied in vitro, using preparations of human umbilical arteries and veins. In addition, the thromboxane formation in human platelets was investigated. Pentoxifylline at 11 mumol/l concentration stimulated PGI2-release from umbilical veins from 14 +/- 8 to 28 +/- 4 pmol/100 mm2 (P less than 0.05). Similarly, pentoxifylline stimulated PGI2-formation in umbilical arteries at 36 and 110 mumol/l concentration from 12 +/- 2 to 23 +/- 10 and 25 +/- 4 pmol/100 mm2, respectively (P less than 0.05). These amounts of pentoxifylline also produced dose-dependent relaxation of venous and arterial vessel strips but did not change the ADP- or collagen-induced platelet aggregation in platelet-rich plasma in vitro. There was no influence by pentoxifylline on the arachidonic acid-induced thromboxane formation of human platelets. These data demonstrate for the first time stimulation of PGI2-formation in human blood vessels by pentoxifylline in vitro. It is suggested, that the antiplatelet effects of pentoxifylline in vivo may be mediated by primary vascular mechanisms.