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This study was designed to assess platelet activity in vivo with vascular prostheses seeded with endothelial cells to determine the time course for development of thromboresistance and to test the ability of prostheses to produce prostacyclin. Sixteen dogs were randomly allocated to receive seeded (experimental group) or unseeded (control group) velour Dacron aortic prostheses. Serial measurements of platelet survival were performed to assess platelet interaction with prostheses in vivo, and platelet serotonin was monitored as an index of platelet release in vivo. After placement of prostheses, dogs in the experimental group had rapid normalization of platelet survival, with most having normal platelet survival at 4 to 8 weeks after surgery. In contrast, most control animals had reduced platelet survival throughout the 12 week period of study. Significant differences between groups in mean platelet survival were noted at 8 weeks after surgery (p < .005) and in mean platelet serotonin at 12 weeks after surgery (p < .05). Luminal surface production of 6-keto-PGF1, from seeded prostheses was similar to aortic production and significantly greater (p < .05) than that of control prostheses. Gross thrombus was present on 6.0 ± 3.4% of the prosthetic surface in experimental animals in comparison to 26.6 + 19.2% in controls (p < .005). The results of these studies document accelerated nonreactivity with platelets of seeded prostheses due to rapid coverage with endothelium possessing a normal ability to produce prostacyclin. Circulation 69, No. 3, 632-639, 1984. PLATELET INTERACTION with vascular prosthetic surfaces is an undesirable process that contributes to occlusive thrombosis and distal embolization.1' 2 After placement of arterial prostheses in man and experimental animals, platelets rapidly and continuously accumulate on the surface.3-' The process can be monitored quantitatively by serial measurement of platelet survival time or by imaging radiolabeled platelets on the surface.6 In dogs, measurement of platelet serotonin also reflects platelet interaction with prosthetic surfaces, and changes in platelet serotonin parallel changes in platelet survival.5 Studies in baboons and dogs have documented that platelet survival, which is

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Di-2-ethylhexyl phthalate and butyl glycolyl butyl phthalate, plasticizers which can be leached into blood from polyvinyl chloridecontaining medical devices, cause significant growth inhibition in cultures of the human diploid cell strain WI-38. The ID50 (dose which causes 50 7,' growth inhibition in tissue culture) values for di-2-ethylhexyl phthalate and butyl glycolyl butyl phthalate were 70 PM and 12 PM, respectively, for WI-38 cells. Toxic effects were greater in a replicating cell population than in a nonreplicating, confluent cell layer. WI-38 cells which were grown in 160 ,UM di-2-ethylhexyl phthalate for 3 days, and subsequently subcultured ' Department of Anatomy.

In order to provide autologous adult endothelial cells for the production of cell-lined artificial vascular prostheses, we have developed a method for harvesting large numbers of cells with minimal contamination by other cellular types. In this technique, the vein is incubated in trypsin-EDTA solution followed by collagenase and the endothelial cells flushed off with a stream of culture medium. With care and appropriate timing, the endothelium can be selectively removed leaving the underlying basal lamina intact.