We have previously reported alterations in
cyclooxygenase metabolism in cultured aortic and pulmonary arterial endothelial cells exposed to acute and chronic
hypoxia. These alterations depended on the duration and degree of the hypoxic exposure, on the vascular bed from which the endothelial cells were derived, and possibly on the availability of
arachidonic acid secondary to modifications in metabolic substrate, membrane
phospholipids, and/or membrane
phospholipase activity. To investigate this last point further, we have compared plasma membrane
phospholipid distribution and
phospholipase activity in cultured aortic and pulmonary arterial endothelial cells exposed to both acute and chronic
hypoxia, using two different precursors (
acetic acid and
arachidonic acid) and three different membrane preparations (cell homogenates, partially purified plasma membranes, and highly purified plasma membranes). We found that exposure to acute and chronic
hypoxia has profound and complicated effects on endothelial cell
phospholipid composition and
phospholipase activity and that these effects depend on the origin of the endothelial cells and the duration of
hypoxia. Furthermore, we found that the alterations in endothelial cell
phospholipid distribution in response to
hypoxia depend on the purity of the plasma membrane preparation and the metabolic precursor used to study
phospholipid metabolism. Finally, these studies suggested that alterations in
phospholipids during
hypoxia occurred to a greater extent in compartments of endothelial cells other than the plasma membranes and that the well-recognized tolerance of endothelial cells to
hypoxia may be due, in part, to preservation of the integrity of their plasma membranes during exposure to acute and chronic
hypoxia.