The prostacyclin stimulating plasma factor activity improves thromboresistance only if vascular PGI2-production is intact.

PGI2 is important in regulating platelet vessel wall interaction (1). In perfusion chamber experiments the amount of PGI2 formed was inversely related to the amount of platelets deposited (2). In 1978 a plasma factor was described which stimulates vascular PGI2-production (3). In later years, this activity has been monitored in different patient groups (for review see 4). Interestingly, it has been found that diseases associated with an increased bleeding tendency such as uraemia (5) or hepatic failure (6) were associated with an increased PF-activity while others with an enhanced thrombophilia sometimes show an absence of PF-activity (7). Recently, the PGI2 stimulating plasma factor has been purified and cloned (8). It was the aim of these experiments to assess whether PF-activity plays a role in local hemostasis regulation under in-vivo flow conditions and whether this is dependent on the presence of an intact PGI2-formation.