Schröer R H
Angiology. 1985 Jun;36(6):387-98. doi: 10.1177/000331978503600608.
An up-dated synopsis is given on the antithrombotic potential of pentoxifylline. Pentoxifylline enhances the PGI2 release from the vascular wall and causes increasing platelet sensitivity to antiaggregating prostaglandins. By its PDE inhibiting effect pentoxifylline in high doses can also enhance PGI2-stimulated cAMP synthesis. These platelet aggregation inhibiting effects in combination with increases in fibrinolytic activity under pentoxifylline administration are suggested to be the main determinants of the compound's antithrombotic properties as evident from investigations in different animal models of thrombosis: Intravascular thrombus formation upon stimulation by both iontophoretically introduced ADP or laser injury of endothelium in the hamster cheek pouch and in the rat mesentery, respectively, was significantly reduced under pentoxifylline. Clinically these findings are corroborated by the regress of platelet aggregability, reduction in fibrinogen, increase in AT III and decrease in antiplasmin activity under treatment with pentoxifylline.
