Abstract
The clinical use of Sodium nitroprusside (SNP) may be associated with an alteration of platelet function. The main focus of this study was the effect of SNP on platelet aggregation in the absence or presence of endothelial cells.Methods: Platelets were incubated with different concentrations of SNP with and without endothelial cells. Platelet aggregation was induced by ADP.Results: Platelet aggregation was significantly inhibited by all concentrations of SNP. Endothelial cells significantly increased this inhibitory effect of SNP. Time course studies showed an inverse correlation of incubation time to platelet aggregation inhibition in the absence of endothelial cells, and a direct correlation in the presence of endothelial cells. Blocking platelet and endothelial cell guanylate cyclase with 1 H-(1,2,4)-oxadiazolo(4,3-a) quinoxalin-1-one (ODQ), or pretreatment of the endothelial cells with cyclooxygenase – inhibitors, had no influence on the increased inhibitory effect of the endothelial cells. Cyanide reversed the inhibitory effect of SNP completely.Conclusion: Endothelial cells play an important role in the SNP mediated inhibition of platelet aggregation. The effect is reversible only by cyanide, not by blocking classical NO signal transduction.
Highlights
The administration of Sodium nitroprusside (SNP) is a highly effective strategy in pulmonary and systemic hypertension crisis, both in adults and in neonates [1,2]
In our study we could clearly demonstrate that endothelial cells play an important role in the antiaggregatory effect of SNP
The Levin study used supernatants of SNP-incubated endothelial cells and did not preincubate the endothelial cells with cyclooxygenase inhibitors, which may have led to different results
Summary
The administration of Sodium nitroprusside (SNP) is a highly effective strategy in pulmonary and systemic hypertension crisis, both in adults and in neonates [1,2]. A well known side effect of NO is the inhibition of platelet function [5,6]. This interference of platelet activation is due to the stimulation of the soluble guanylate cyclase which increases the concentration of cGMP and inhibits the calcium-dependant platelet activation [7]. Just recently Jensen et al published a study on the potential synergistic effect of Dipyridamole and NO donors, such as sodiumnitroprusside, to prolong the inhibition of thrombin-induced platelet shape change. Just recently Jensen et al published a study on the potential synergistic effect of Dipyridamole and NO donors, such as sodiumnitroprusside, to prolong the inhibition of thrombin-induced platelet shape change. [8]
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