-20.3 ± 5.3%; P 2-dependantplatelet aggregation, celecoxib had a modest but significant inhibitoryeffect on serum TxB2 4 hr after dosing.
By contrast, bothibuprofen and celecoxib suppressed a biochemical index of COX-2 activity(endotoxin induced PGE2 in whole blood ex vivo) to acomparable degree (-93.3 ± 2% vs.
JF - Behavioural Brain Research
The light dark (LD) test was used to further assess anxiety-like behavior by observing the naturalistic conflict between the tendency to explore a novel environment rather than the aversive brightly lit open-field. At 3 months, there were no significant differences in either the time spent in the lit area or number of transitions (). At six months of age PGIS mice significantly spent more time in the lit are and made fewer transitions (, p
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Reductions in prostacyclin production inseveral diseases, including atherosclerosis and diabetes, have beendescribed and implicated in the pathophysiology of these diseases.
, Roland W. Moskowitz, Aviv Hassid
Additionally, since prostacyclin powerfully inhibits plateletaggregation and promotes their disaggregation, this agent could have animportant use in the therapy of conditions in which increased plateletaggregation takes place and in which, perhaps, a prostacyclin deficiencyexists.
/ ; Moskowitz, Roland W.; Hassid, Aviv.
Prostacyclin has been used beneficially in humans duringextracorporeal circulation procedures such as cardiopulmonary bypass,charcoal haemoperfusion and haemodialysis.
JO - Journal of Cellular Physiology
Thesedata suggest that (i) platelet COX-1-dependent aggregation is notinhibited by up to 800 mg of celecoxib; (ii) comparable COX-2 inhibitionis attained by celecoxib (100-800 mg) and ibuprofen (800 mg) after acutedosing; and (iii) COX-2 is a major source of systemic prostacyclinbiosynthesis in healthy humans.
JF - Journal of Cellular Physiology
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1 Dipyridamole (0.01 to 0.75 mM) increased prostacyclin (PGI2) biosynthesis from tritiated arachidonic acid in rat stomach fundus homogenates by 21 to 350%. The transformation of prostaglandin H2 (PGH2) to PGI2 by a microsomal fraction of pig aorta was stimulated by dipyridamole at 0.1 M by 63%. 2 In the isolated perfused heart of the rabbit dipyridamole at 1 and 5 micrograms/ml increased PGI2 release by 70% and 146% respectively. 3 Our results show a stimulation of the second step in PGI2 biosynthesis (from endoperoxides) by dipyridamole. This effect should be considered in relation to the therapeutic usage of the drug in myocardial infarction.