This paper reviews pathophysiological processes occurring after contact of
blood with artificial surfaces and the predominant role of platelets in the
genesis of extracorporeal thrombosis. Bleeding complications are common du
ring conventional heparin anticoagulation, and both clinical and experiment
al evidence suggests that the efficacy of heparin as an anticoagulant is co
mpromised by its relative ineffectiveness towards platelets. Consequently,
drugs that inhibit interaction between platelets and artificial membranes h
ave been introduced as an alternative anticoagulant strategy. This paper re
views studies on the use of short-acting antiplatelet prostaglandins such a
s prostacyclin and prostaglandin E-1 alone or in combination with heparin d
uring various forms of extracorporeal circulation such as cardiopulmonary b
ypass, haemodialysis, continuous haemofiltration, membrane oxygenation, ven
tricular assist devices, and haemoperfusion. Temporary paralysis of platele
t function with antiplatelet prostaglandins has been effective in controlli
ng platelet-surface interaction and reducing bleeding complications and mor
bidity during and after extracorporeal circulation. By inhibiting the forma
tion of fibrin, leukocyte and platelet-based microaggregates and cytoprotec
tive actions, prostaglandins have been shown to prevent renal, neurologic,
and pulmonary dysfunction after extracorporeal circulation. Prostaglandins
were most effective in increasing the biocompatibility of extracorporeal sy
stems when they were administered as a supplement to but not as a substitut
e for heparin. The use of prostaglandins alone should be reserved for patie
nts who are resistant to heparin or heparin-induced thrombocytopenia.