Abstract
Diamide elicits initial stimulative and delayed inhibitory effects on the aggregation of citrated platelet-rich plasma (PRP). Diamide (50 μM-5 mM) produces shape change and Ca 2+-dependent aggregation, which both are inhibited by prostaglandin E 1 and cytochalasin B (60μM). Enhanced aggregation occurs when diamide is added to PRP simultaneously with ADP or collagen. The resulting aggregation, as well as aggregation caused by diamide alone, turns into disaggregation about 2 min after application of the aggregating agents. The increase of ADP aggregation is restricted to the primary wave. Release of 3H-serotonin and secondary aggregation are inhibited by ≥ 10 μM diamide. Prior exposure of platelets to diamide (100 μM) leads to inhibition of collagen aggregation but not of ADP aggregation, though disaggregation occurs in both cases. The effects of diamide on platelet function may be mediated by lipid peroxides. Their accumulation is probably modulated by glutathione through glutathione peroxidase.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
