Prostacyclin production at the human microvascular anastomosis: its effect on initial platelet deposition

The human microvascular anastomosis represents a localized environment with strongly thrombotic tendencies. In previous studies, an increase in initial platelet deposition at a human ex vivo anastomosis was measured. It is postulated that this increase in anastomotic platelet deposition was due to a reduction in anastomotic prostacyclin production as a consequence of local endothelial cell injury or loss. Instead, in this study, an increase in anastomotic prostacyclin production over unsutured controls (control 1093 +/- 222 pg/ml of 6-keto prostaglandin F (PGF) 1-alpha, n=21; anastomosis 2494 +/- 414, n=21, mean +/- 1 SEM, p=0.005) is demonstrated. Anastomotic prostacyclin production was augmented by addition of arachidonic acid (0.1 mM) (39,000 +/- 11,300 pg/ml of 6-keto PGF 1-alpha, n=7, p<0.001) and suppressed by the preincubation of vessel segments with aspirin in a dose-dependent fashion (1mM) (83+/-22 pg/ml of 6-keto PGF 1-alpha, n=21, p<0.001); aspirin (0.1 mM) (312 +/- 56 pg/ml of 6-keto PGF 1-alpha, n=7, p<0.001). In further studies using a perfusion apparatus of human blood pumped through human placental artery segments, suppression of prostacyclin production did not augment initial platelet deposition (control anastomosis 4.9 +/- 2.2 x10(6) platelets per cm2, aspirin treatment 6.0 +/- 2.8 x 10(6) platelets per cm2, n=5, mean +/- 1 SEM, p>0.05). Suppression of platelet function with aspirin (0.1 mM) also did not decrease initial platelet deposition onto the anastomosis (5.8 +/- 2.8 x 10(6) platelets per cm2, n=r, p>0.05). In this model system, initial platelet deposition at the anastomosis may not be dependent upon cyclooxygenase pathways.