Despite evidence of elevated levels of tissue factor and platelet binding b
y apoptotic endothelial cells, microthrombi do not appear to be associated
with apoptotic endothelium and this suggests maintained anti-aggregatory ac
tivity for platelets. We report that anti-aggregatory activity is maintaine
d by apoptotic endothelium obtained by serum and or matrix deprivation, whi
ch we propose as models for apoptotic endothelial cells released during mic
rovascular remodelling and traumatic detachment respectively. Both apoptoti
c and non-apoptotic endothelium had strong anti-aggregatory activity for pl
atelets stimulated with either ADP or thrombin. Inhibition experiments usin
g L-NAME and indomethacin indicated a role for nitric oxide and prostacycli
n in this activity. Experiments with latex beads further confirmed that inh
ibited platelet aggregation by endothelium was not merely a non-specific ph
enomenon. These data support the idea that EC maintain active antithromboti
c activity during apoptosis, consistent with maintained urokinase levels an
d canalicular fragmentation reported elsewhere.