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 mea sured. It is postulated that this increase in anastomotic platelet dep osition 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 u nsutured 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 w as augmented by addition of arachidonic acid (0.1 mM) (39,000 +/- 11,3 00 pg/ml of 6-keto PGF 1-alpha, n = 7, p < 0.01) and suppressed by the preincubation of vessel segments with aspirin in a dose-dependent fas hion (1 mM) (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 prosta cyclin production did not augment initial platelet deposition (control anastomosis 4.9 +/- 2.2 x 10(6) platelets per cm(2), aspirin treatmen t 6.0 +/- 2.8 x 10(6) platelets per cm(2), 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 cm(2), n = 4, p > 0.05. In this model syste m, initial platelet deposition at the anastomosis may not be dependent upon cyclooxy-genase pathways.