ABSTRACT
Infusion of PGI2 at a dose of 5 or 10 ng/kg/min during 72 hours into patients with peripheral vascular disease was followed by increased susceptibility of platelets to proaggregatory action of ADP and collagen but not that of arachidonate. The above effects were observed 24 hours after termination of infusion of PGI2. A tendency to an increased formation of TXA2 in PRP aggregated by arachidonate was also noticed. Infusion of PGI2 at a dose of 2 mg/kg/min during 72 hours into the patients caused the decreased platelet aggregability to ADP and arachidonate but not to collagen, and a decreased tendency to production of TXA2 in PRP aggregated by arachidonate. The existence of a "rebound effect" in platelets after a long term PGI2 therapy is suggested.
Subject(s)
Arteriosclerosis Obliterans/blood , Blood Platelets/metabolism , Epoprostenol/therapeutic use , Platelet Aggregation/drug effects , Prostaglandins/therapeutic use , Thromboangiitis Obliterans/blood , Adenosine Diphosphate/pharmacology , Adult , Aged , Arachidonic Acid , Arachidonic Acids/pharmacology , Arteriosclerosis Obliterans/drug therapy , Blood Platelets/drug effects , Collagen/pharmacology , Epoprostenol/administration & dosage , Female , Humans , Middle Aged , Thromboxane A2/biosynthesisABSTRACT
In patients with peripheral vascular disease and in healthy rabbits, infusion of PGI2 but not of 6-keto PGF1 alpha induced a rise in blood glucose level and a pathological deviation in glucose tolerance test. In experiments in vitro, the increased concentrations of glucose produced dose-dependent inhibition of PGI2 release from isolated rat aortic rings. The link between PGI2 and carbohydrate metabolism is discussed.
