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.
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.
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