Red blood cell (RBC) effects on platelet adhesion to a nonbiologic test surface (tetrafluoroethylene propylene copolymer) and platelet aggregation during laminar shear flow for shear rates to 5,680 s-1 (corresponding to shear stress to 200 dyne/cm2) were investigated. Results on hemoglobin (Hb) and adenosine diphosphate (ADP) release from RBCs, percent decrease of single platelets in the bulk, and percent of test surface covered with platelets were obtained in a cone-and-plate (CP) viscometer for samples of whole blood, suspensions of RBC ghosts in platelet-rich plasma (PRP), and suspensions of RBCs in either PRP or platelet-poor plasma. Results obtained over the shear rate range studied for samples of normal hematocrit indicated that low-stress shearing led to ADP and Hb release from intact RBCs; shear-induced release of ADP from RBCs was about twice that of platelets, and of the total ADP released, the ADP released from RBCs contributed about six times that of the platelets to single platelet reduction in the bulk and about twice that of the platelets to platelet adhesion, ie, coverage of the test surface with platelets. Results obtained for various hematocrits showed that above a threshold hematocrit of about 25% to 35% the RBCs (suspended in PRP) had a greater contribution to ADP release, platelet adhesion, and platelet aggregation than the platelets themselves. Single platelet reduction for samples of RBC ghosts suspended in PRP correlated with shear rate level and not with shear stress.

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We evaluated the adherence of indium 111-radiolabeled endothelial cells to fibronectin-treated expanded polytetrafluoroethylene surfaces exposed to high (437 s-1) vs low (218 s-1) shear and the influence of shear on prostacyclin production. Canine jugular vein factor VIII-positive endothelial cells in passages 3 through 6 were incubated with 111Indium-oxine, and labeled cells were seeded onto fibronectin-treated expanded polytetrafluoroethylene patches. Patches with confluent cells were exposed to shear in a Weissenberg rheogoniometer for intervals ranging up to 60 minutes. Percent endothelial cell retention was determined by gamma counting of patches and media and by histologic evaluation. Prostacyclin production (tritiated radioimmunoassay of 6-keto-prostaglandin F1 alpha) was assayed on perfusing media. Results showed no differences in 6-keto-prostaglandin F1 alpha production between shear rates or time periods. Endothelial cell retention did not differ between the shear rates. Rotational shear caused persistent cell loss over time in either high- or low-shear conditions. This persistent cell loss in response to steady rotational shear differs from that in response to identical rates of pulsatile linear shear in our laboratory where cell loss approached zero after 15 minutes.