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Imparied platelet--dense granule release in neonates
P Mankin1, J Maragos, M Akhand
1Pediatrics Department, University of Illinois College of Medicine at Peoria, USA.
Insights
Infant platelets show impaired dense granule release compared to adults, suggesting a potential cause for their reduced response to certain stimuli. This difference in platelet dense granule (PDG) release may impact infant hemostasis.
Area of Science:
- Hematology
- Neonatal Physiology
- Platelet Biology
Background:
- Platelet dense granules (PDGs) are crucial for hemostasis, releasing key molecules like ATP upon activation.
- Infants, particularly preterm infants, exhibit altered platelet function compared to adults.
- Understanding these differences is vital for managing neonatal bleeding risks.
Purpose of the Study:
- To investigate differences in platelet dense granule (PDG) uptake and release.
- Compare PDG function between preterm infants, term infants, and adults.
Main Methods:
- Flow cytometry was used to assess PDG uptake and release.
- Mepacrine fluorescent staining was employed on platelets from term infants, preterm infants, and adults.
- Platelets were stimulated with thrombin to evaluate responses.
Main Results:
- Initial mepacrine uptake by infant platelets was comparable to adult platelets.
- Significant differences in PDG response to thrombin stimulation were observed between infants and adults.
- Infant platelets showed persistent mepacrine staining after stimulation, unlike adult platelets.
Conclusions:
- Defective PDG release in infants is suggested by persistent mepacrine staining post-thrombin stimulation.
- Impaired PDG release may contribute to infants' reduced response to agonists requiring ATP release.
- This finding has implications for understanding neonatal hemostatic challenges.
Purpose:
The aim of this study is to examine differences in platelet dense granule (PDG) uptake and release between preterm infants, term infants, and adults.
Methods:
PDG uptake and release was examined by flow cytometry using mepacrine fluorescent staining in phycoerythrin-anti-GPIIb/IIIa bound platelets taken from cord blood of eight term infants and seven preterm infants and venous blood from eight adults.
Results:
Analysis of the baseline fluorescence in the untreated versus thrombin-treated samples revealed significant differences in the way infant PDGs responded to thrombin stimulation when compared with adults. Initial uptake of mepacrine in both term and preterm platelets was similar to that in adult platelets. Statistically significant differences between adults and both term and preterm infants, at two concentrations of mepacrine, were observed after stimulation with thrombin.
Conclusion:
Persistent mepacrine staining of infant PDGs, when compared with those of adults, after thrombin stimulation implies defective infant PDG release. This may partially explain why infants have impaired response to agonists requiring ATP release from PDGs.