[Role of cytosolic calcium balance on cell injury in cultured bovine aortic endothelial cells during hypoxia and reoxygenation].

Making use of an in vitro model of bovine aortic endothelial cell monolayers, the cell viability and changes of intracellukar calcium concentration of the preparation were submitted to hypoxia with or without reoxygenation. It was shown that the cell viability declined under hypoxia but increased under reoxygenation when the endothelial cells were incubated in calcium-free HBSS, as compared with control HBSS incubation. It was observed that a significant reduction of intracellular calcium from 99 to 69 nmol/L during 2 h of hypoxia, which was further decreased in Ca(2+)-free HBSS medium. After 4 h hypoxia followed by 40 min reoxygenation, [Ca2+]i recovered to the nomal concentration. It is speculated that the calcium homeostasis may be an important condition for cells to carry out normal function and either decrease or increase of [Ca2+]i may injury bovine aortic endothelial cells.