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Aggregation of platelets in whole blood from children with pulmonary hypertension
Insights
Platelet aggregation response to adenosine diphosphate was reduced in children with pulmonary hypertension. Lowering hematocrit improved response, suggesting red blood cells may interfere with platelet function.
Area of Science:
- Hematology
- Pediatric Cardiology
- Platelet Physiology
Background:
- Pulmonary hypertension can affect blood components.
- Platelet function is crucial for hemostasis and can be altered in disease states.
Purpose of the Study:
- To assess platelet aggregation response to adenosine diphosphate and collagen in children with pulmonary hypertension.
- To investigate the impact of hematocrit on platelet function in this population.
Main Methods:
- Whole blood impedance method used to measure platelet aggregation.
- Platelet aggregation assessed in response to adenosine diphosphate and collagen.
- Hematocrit adjusted in vitro using autologous platelet-rich plasma.
Main Results:
- Platelet response to collagen was normal in children with pulmonary hypertension.
- A decreased platelet response to adenosine diphosphate was observed, particularly at high inducer concentrations.
- In vitro reduction of hematocrit increased platelet count and partially restored adenosine diphosphate-induced aggregation.
Conclusions:
- Platelet aggregation is relatively preserved in children with pulmonary hypertension.
- Reduced adenosine diphosphate response may be linked to high hematocrit and red blood cell interference.
- Potential leakage of endogenous adenosine diphosphate from red blood cells might contribute to a refractory state in platelets.
Abstract:
The response of aggregation of platelets to adenosine diphosphate (7.5-120 microM) and collagen (1.25 micrograms/ml) was assessed in whole blood (impedance method) in 10 children with pulmonary hypertension (hematocrit range, 42 to 71%). The response to collagen was normal (9.08 +/- 3.47 vs. 10.36 +/- 1.86 ohms in controls, P = NS) while there was a decreased response to adenosine diphosphate (6.98 +/- 3.83 vs. 11.21 +/- 2.02 ohms, P less than 0.01), in spite of high concentrations of the inducer. Lowering the hematocrit in vitro to 40% with autologous platelet-rich plasma resulted in a rise in the platelet count from 171 +/- 63 to 225 +/- 84 x 10(9) platelets/1 (P less than 0.001) and a significant increase in the response to adenosine diphosphate from 6.98 +/- 3.83 to 9.89 +/- 3.66 ohms (P less than 0.02). As in the baseline condition, high concentrations of adenosine diphosphate were required. The response to collagen did not change significantly. The results indicate that aggregatory response of platelets is relatively preserved in these children. The decreased response to adenosine diphosphate may be a result of a low count and interference of red cells on the accretion of platelets on the electrodes. Because high concentrations of adenosine diphosphate were still required after hemodilution to achieve an aggregatory response close to normal, we speculate that leakage of endogenous adenosine diphosphate from red cells may have accounted for partial activation of the platelets, resulting in a relative refractory state to in vitro stimulation.