EFFECTS OF I.V. AND I.A. PGE1-INFUSION IN DIFFERENT DOSES ON FIBRINOLYTIC ACTIVITY, PLATELET FUNCTION AND STABLE PGE1 METABOLITES

As it is well known that PGE1 is degraded during lung passage to a major extent, we examined what the optimal route and dosage concerning platelet function and plasmatic coagulation would be.

6 patients with peripheral vascular disease (PVD) stage lib according to Fontaine were treated either i.a. (1,25 or 2,50 ng PGE1 [Prostavasin]/kg/min) or i.v. (5 or 10 ng/PGEl/kg/min) for 120 minutes.Various parameters reflecting platelet function (βTG, PF4, serum TXB2, ADP-induced aggregation, platelet sensitivity to PGI2, intraplatelet cAMP) plasmatic coagulation and fibrinolytic activity were measured. Blood was drawn from the contralateral cubital vein avoiding occlusion before and 5,30,120,125 and 185 minutes after starting PGE1. Fibrinopeptide A (1,03±0,38 → 2,57±1,32; p<0,01), plasminogen (108,5+10,7 → 1,24±11,5; p<0,01), plasmin changed, whereas α2-anti-plasmin tissue plasminogen activator (72,7±34,7 → 94,0±32,5) and urokinase did not change (1,00±.0,41 → 1,30±0,95) significantly. The long-lasting influence on the fibrinolytic activity can not be explained by a direct action of PGE1 or 15-keto-13,14 DH-PGE1. RIA determination of 15-keto-13,14 DH-PGE1 exhibited a certain dose-dependent effect of PGE1 on the plasma levels of the immunoreactive substance. The findings are suggestive for a process persisting even after complete disappearance of the causative agent, or for a biological capacity of a so far unknown long-lived PGEl-metabolite. PGE1 did not significantly affect the platelet function parameters.