Platelet Protection and Heparin Sparing With Prostacyclin During Regular Dialysis Therapy

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

“…This effect has been looked for but not seen consistently in patients undergoing cardiopulmonary bypass Longmore et al, 1981;Walker et al, 1981) or charcoal haemoperfusion; this may be because the agent responsible is being destroyed or removed , or because in these circumstances flushing seems too minor an effect to warrant comment. Facial flushing can also occur during haemodialysis with PGI2 (Turney et al, 1980;Zusman et al, 1981b) and has also been seen following inhalation of PGI2 (Bianco et al, 1979;Szczeklik et al, 1978b). Flushing is seen in the affected limb when PGI2 is infused intra-arterially (Machin et al, 1981b).…”

Use of a thromboxane synthetase inhibitor, dazoxiben, during haemodialysis.

“…However, it is important to note that the fall in the platelet count was much less than we have previously observed (Turney et al, 1980). This may be related to the type of dialyser and perhaps to the particular batch of heparin used.…”

“…Lindsay et al (1972b) have also reported that aspirin and dipyridamole protected the platelets and reduced dialyser blood loss. We have reported platelet sparing activity and reduced dialyser fibrin deposition with sulphinpyrazone (Woods et al, 1979), and more recently shown that prostacyclin can minimize platelet loss and reduce heparin requirement during regular haemodialysis (Turney et al, 1980). Surface contact activation of platelets in the extracorporeal circulation may lead to an accumulation of prostacyclin endoperoxides, PGG2 and PGH2, which are then converted to thromboxane A2 (TXA2) by the enzyme thromboxane synthetase, promoting platelet aggregation.…”

Effect of Inhibition of Prostaglandin Synthesis on Platelet Count, Platelet Aggregates and Arterial Oxygen Tension during Hemodialysis

“…Interaction between blood and foreign surfaces during hemodialysis causes release o f platelet proteins and thrombocytopenia [5], increase in plasma thromboxane metabo lites [6] and circulating platelet aggregates [7][8][9] in arterial blood and in the effluent from the artificial kidney. The increase in circulat ing platelet aggregates reaches a maximum coincidently with the drop in arterial oxygen tension, suggesting that pulmonary emboli zation of these may be contributing to dialy sis-induced hypoxemia [7,8].…”

“…Coincidently with the hypoxemia throm bocytopenia [5], increase in plasma throm boxane metabolites [6], and increase in circu lating platelet aggregates [7][8][9] occurs.…”