Pharmacological Effect of Nitroprusside on Platelet Aggregation

Abstract

Adequate platelet function and numbers are critical for postcardiopulmonary bypass patients. Endogenous and pharmacological sources of nitric oxide (NO) are known inhibitors of platelet aggregation. Sodium nitroprusside (SNP), used clinically to control blood pressure, is an inorganic source of NO. Our long-term goal is to determine if SNP infusion in the venous return line of the cardiopulmonary bypass system would preserve platelet numbers and function without affecting systemic vascular resistance. Our first requirement to accomplish this goal was to develop an assay that would detect the SNP effect on platelet aggregation. We, therefore, tested the hypothesis that clinical concentrations of SNP would inhibit platelet aggregation. We quantified platelet aggregation with the Medtronic Hepcon HMS whole blood aggregometer. Normal heparinized human blood was treated with 0.625 to 12.5 nM platelet activating factor (PAF), 0.25 to 5.0 µM epinephrine, or 0.20 to 10 µM adenosine 58-diphosphate (ADP) to stimulate platelet aggregation. SNP was added at 10−5 M to determine its affect on PAF, epinephrine, and ADP stimulated platelet aggregation. The results demonstrated that PAF-stimulated platelet aggregation was significantly inhibited with SNP (10−5 M) to 82% (p < .05) of control and epinephrine and ADP mediated aggregation were not significantly affected. In conclusion, at clinically relevant concentrations SNP inhibits platelet aggregation by PAF but not with ADP or epinephrine.