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) I-alpha, n = 2); 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 I-alpha, n = 7, p < 0.01) and suppressed by the preincubation of vessel segments with aspirin in a dose- dependent fashion (1 mM) (83 ± 22 pg/ml of 6-keto PGF I-alpha, n = 21, p < 0.01); aspirin (0.1 mM) (312 ± 56 pg/ml of 6-keto PGF I-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 x 106 platelets per cm2, aspirin treatment 6.0 ± 2.8 x 106 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 ± 106 platelets per cm2, n = 4, p > 0.05. In this model system, initial platelet deposition at the anastomosis may not be dependent upon cyclooxygenase pathways.
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