The relative roles of blood cell products and plasma factors on endothelial cell proliferation were evaluated by studying the proliferative response of human umbilical vein endothelial cells to cell free plasma derived serum (CFPDS), whole blood serum (WBS), platelet released factors, fibroblast growth factor and macrophage conditioned medium in vitro. Human adult arterial smooth muscle cells were treated in a similar manner for comparison. The rate of endothelial cell proliferation was directly related to the concentrations of both WBS and CFPDS. Grwoth rate in WBS was marginally greater than that observed in CFPDS during early culture, however, similar confluent densities were achieved. The addition of platelet released factors to CFPDS did not further stimulate endothelial cell proliferation. In contrast smooth muscle cells were quiescent in CFPDS despite increasing serum concentrations, but proliferated actively in response to platelet released factors. Both human macrophage conditioned medium and fibroblast growth factor increased endothelial cell proliferation significantly when compared with CFPDS alone. It is concluded that endothelial cell proliferation in preconfluent cultures is dependent on plasma factors while human vascular smooth muscle cells also require cell derived mitogens such as platelet growth factor to proliferate. The release of a substance by human macrophages mitogenic for endothelial cells may be involved in endothelial cell proliferation in vivo.

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The in vitro immune response of uremic and transplanted patients was studied by determining lymphocyte surface and functional markers. Because of lymphopenia, the absolute number of T and B cells are diminished in uremia and transplantation. The uremic state had a profound effect of T cell mitogenic response, while the relative number (%) of T cells was not reduced. B cell responses and relative numbers were significantly diminished. The early posttransplant period was associated with a significant reduction in both T and B cell response and relative numbers. All indexes returned toward normal late in the posttransplant course with reduction of immunosuppression and cessation of the uremic state. Horse anti-human lymphocyte globulin treatment caused a significant reduction in T cells and an increase in B cells. Prednisone therapy did not appear to influence the relative number of the lymphocyte subpopulation but did reduce the mitogenic responses. Changes in surface or functional markers did not prove useful in predicting rejection episodes in transplanted patients.