Antiplatelet Effects of Sodium Nitroprusside in Flowing Human Blood: Studies under Normoxic and Hypoxic Conditions

Abstract

We explored the ability of sodium nitroprusside to modify adhesive and cohesive function of platelets in flowing blood, under normoxic and hypoxic conditions. Aliquots of both untreated and sodium nitroprusside–treated blood were prepared for studies of: (1) platelet aggregation in plasma; (2) erythrocyte deformability; (3) platelet interaction with damaged subendothelium, by using a well-defined perfusion system; and (4) blood gasometry in the perfused samples. Results showed that sodium nitroprusside–treated blood always showed a totally inhibited arachidonic acid–induced platelet aggregation in plasma, as well as significantly increased erythrocyte deformability (0.44±0.09 up to 0.66±0.05; p<0.05). However, treatment with sodium nitroprusside did not modify the pattern of platelet interaction with subendothelium (percentage of contact, adhesion, thrombus, and covered surface) with respect to untreated blood, under any of the shear rates used (300, 800, and 1800 seconds −1), although it significantly reduced the height of thrombi (9.8±0.4 vs. 8.3±0.4 μm; p<0.05). Hypoxic conditions did not have a noticeable effect in modifying antiplatelet effects of sodium nitroprusside. Additionally, the presence of sodium nitroprusside impaired the normal oxygenation of the blood during perfusion. pO 2 in control untreated samples rose from 40.3±5.0 mm Hg perfusions to 100.4±12.5 mm Hg but remained at 66.3±6.3 mm Hg in sodium nitroprusside–treated blood ( p<0.05). Our results did not show a significant effect of sodium nitroprusside in the modulation of platelet interaction with subendothelium. The marginal reduction in the thrombi height could be related to rheological interference of increased erythrocyte deformability.