The objective of this research will be to determine: (1) How oxidants (i.e. oxygen-derived free radicals) effect the transport of 5-hydroxy-tryptamine (5-HT) in pulmonary endothelial cells. (2) The possible role that 5-HT plays as an endogenous oxidant protecting agent in pulmonary endothelial cells. (3) The effect of free radicals on the snythesis of prostacyclin in endothelial cells. (4) Is there a correlation between update of 5-HT into endothelial cells and the synthesis or release of prostacyclin. Both cultured pulmonary endothelial cells and intact animals will be utilized in this project. Data obtained in this proposal will then be extended to determine how damage to the pulmonary endothelium may effect biochemical processes in other cell types within the microvasculature (i.e. smooth muscle cells and connective tissue fibroblasts). Furthermore, data obtained in this proposal can be extended to other tissue microvasculature systems in which endothelial cells appear to be the initial cell type affected. This is especially true in pathological processes, which involve the immune system, since these cells elaborate large amounts of oxygen free radicals as one of their functions.
| Kwock, L; Davenport, W C; Clark, R L et al. (1987) The effects of ionizing radiation on the pulmonary vasculature of intact rats and isolated pulmonary endothelium. Radiat Res 111:276-91 |
| Friedman, M; Saunders, D S; Madden, M C et al. (1986) The effects of ionizing radiation on the pulmonary endothelial cell uptake of alpha-aminoisobutyric acid and synthesis of prostacyclin. Radiat Res 106:171-81 |
| Friedman, M; Madden, M C; Saunders, D S et al. (1985) Ozone inhibits prostacyclin synthesis in pulmonary endothelium. Prostaglandins 30:1069-83 |
