The effects of estrone, estradiol and estriol on platelet aggregation induced by adrenaline and adenosine diphosphate
Department of Pharmacology, Faculty of Medicine Siriraj Hospital, Mahidol University, Prannok Rd, Bangkok 10700, Thailand. Platelets
(Impact Factor: 2.98).
12/2006; 17(7):441-7. DOI: 10.1080/09537100600745302
The impact of estrogens on the cardiovascular system and their ability to regulate platelet functions remains controversial. Changes in platelet functions could contribute to thrombotic risk associated with estrogen treatments. Here, we investigated the effects of various forms of estrogen, including estrone (E1), estradiol (E2) and estriol (E3), on platelet aggregation induced by standard agonists (adrenaline and adenosine diphosphate). Platelet-rich plasma (PRP) was prepared from citrated blood donated by 25 normal volunteers. The study on platelet aggregation was carried out in 96-well flat-bottom microtitre plates and assessed using a microplate reader. For studying the effects of each estrogen, PRP was preincubated with 1, 10 and 100 nM of E1, E2 and E3 at 37 degrees C for 20 min, and then coincubated with normal saline (control untreated PRP), adrenaline (ADR) or adenosine diphosphate (ADP) in the microplate. Platelet aggregation was then measured every minute for 8 min. None of the estrogens (E1, E2 and E3) affected platelet aggregation in untreated PRP. Interestingly, only E1 and E3 can synergize the increased platelet aggregation by either ADR or ADP, while the effects of E2 on the increased platelet aggregation by either ADR or ADP depended on internal factors such as endogenous estradiol and platelet aggregated state. Thus, for the rational use of these internal factors for estrogen use, especially E2, in clinical applications, such as hormone replacement therapy, may need evaluation of thrombotic risk.
Available from: Peter Rubak
- "Melamed et al. suggested that the gender differences might be caused by estrogen   . However, studies on this hypothesis are scarce and conflicting     . "
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ABSTRACT: Analyses of platelet aggregation in hirudin whole blood using Multiplate® was validated. Reference intervals for the most commonly used agonists were established, and the association between platelet aggregation, age, gender and haematological values was analysed.
We included 121 healthy individuals to establish reference intervals and six healthy individuals for evaluation of the day-to-day variation. Platelet aggregation was evaluated on hirudin whole blood employing Multiplate® induced by arachidonic acid, ADP, collagen and ristocetin (RISTOlow and RISTOhigh). Measurements of haematological values were performed employing Sysmex K-4500.
We found no association between platelet aggregation and age (p>0.57 for all agonists, except RISTOlow: p=0.05). Platelet aggregation was significantly higher in women compared to men for all agonists (p<0.0003), except RISTOlow (p=0.05). A reference interval is presented as 95% confidence interval suitable for any age and both sex. Day-to-day variation was <11% for all agonists except for RISTOlow. No association was found between platelet aggregation and haematocrit or red blood cell count after adjusting for age and gender except for RISTOhigh. A positive significant association was found between platelet count and platelet aggregation (p<0.04). Finally, a significant positive association was found between platelet aggregation and white blood cell count for all agonists (p<0.05) except RISTOlow and RISTOhigh (p>0.05).
Reference intervals for platelet aggregation in healthy individuals (age: 17 to 66 years) were established in hirudin whole blood measured by Multiplate® employing the most commonly used agonists.
Thrombosis Research 07/2012; 130(3):420-3. DOI:10.1016/j.thromres.2012.06.017 · 2.45 Impact Factor
Available from: liu.diva-portal.org
Available from: Joe Raya
Journal of Thrombosis and Haemostasis 05/2008; 6(4):703-5. DOI:10.1111/j.1538-7836.2008.02898.x · 5.72 Impact Factor
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