Impaired mobilization of intracellular calcium in neonatal platelets.

Abnormalities in platelet functions including aggregation and the release reaction have long been recognized to be present in neonatal platelets. Because calcium is an important mediator of many platelet functions, we have investigated the mobilization of calcium in neonatal platelets. All umbilical cord blood samples were obtained from healthy, full term gestations. Changes in cytoplasmic calcium levels were monitored using Fura-2 as a fluorescent probe. Fura-2-loaded washed platelets were stimulated with the agonists collagen (2 micrograms/mL) or thrombin (1.0 U/mL). When compared with adult controls, intracellular calcium release in the platelets of the neonate was significantly impaired in response to these agonists. Mean levels for calcium release in adults versus neonates in response to collagen were 168 +/- 120 nM (+/-SD, n = 10), and 61 +/- 69 nM (n = 7, p < 0.05). A decrease in response to thrombin was also observed [1296 +/- 503 nM (n = 8) in adults versus 603 +/- 482 nM (n = 7) in neonates, p < 0.025]. Results similar to those observed with unpaired neonatal and adult platelets were also obtained when neonatal platelets (n = 5) were compared with their paired maternal controls. In further studies, we have documented that the calcium content of the dense tubular system was normal in the neonatal platelet, indicating that the observed impairment in calcium mobilization in the neonate was not due to a decrease in calcium stores. The previously documented abnormalities in neonatal platelet function appear to be due to the impaired mobilization of this important intracellular mediator.