AJP - Cell Physiology, Vol 259, Issue 5 C738-C745, Copyright © 1990 by American Physiological Society
Reduced prostacyclin formation after reoxygenation of anoxic endothelium
S. L. Hempel, D. L. Haycraft, J. C. Hoak and A. A. Spector
Department of Internal Medicine, University of Iowa, Iowa City.
Human umbilical vein endothelial cells subjected to 24 h of anoxia followed
by reoxygenation released less prostacyclin (PGI2) in response to thrombin,
calcium ionophore A23187, or arachidonic acid. This was associated with a
substantial increase in stimulated platelet adherence. Increased lactate
dehydrogenase and 51Cr release occurred after 1 h of reoxygenation, but the
high rate of release did not persist during the subsequent 23 h of
reoxygenation. The changes in platelet adherence and PGI2 release partially
resolved over 24 h. PGI2 formation from prostaglandin H2 was not reduced,
suggesting that cyclooxygenase activity, but not prostacyclin synthase, is
affected by reoxygenation. A decrease in arachidonic acid release from
cellular lipids also occurred. The reduction in cyclooxygenase activity,
but not arachidonic acid release, was prevented by the presence of
ibuprofen during reoxygenation. Addition of catalase or superoxide
dismutase during reoxygenation increased PGI2 release but did not
completely overcome the reduction relative to control cultures. These
findings suggest that the increase in platelet adherence during
reoxygenation may be mediated in part by a change in cyclooxygenase
activity. This is only partly overcome by extracellular oxygen species
scavengers but is prevented by the presence of a reversible cyclooxygenase
inhibitor during reoxygenation.
