Effects of sodium nitroprusside on hemodialysis-induced platelet activation

Background. Hemodialysis (HD) is associated with increased platelet activat ion as reflected by enhanced P-selectin expression on platelets and by incr eased formation of heterotypic platelet-leukocyte aggregates. Both may play a pathophysiologic role in HD-associated platelet dysfunction or the propa gation of atherosclerosis. As nitric oxide (NO) is a potent inhibitor of pl atelet activation, we were interested in whether HD-induced platelet activa tion could be blunted by a NO donor. Methods. After a pilot study in 12 patients to gain an estimate for the sam ple size, the main trial was conducted as a randomized, double-blind, place bo-controlled, two-way, crossover study. Twelve patients received an infusi on of sodium nitroprusside (1 mu g/kg/min for over 15 min) or placebo into the inlet port of the HD device. Results. Platelet activation increased within five minutes after start of H D (P < 0.05). Infusion of sodium nitroprusside neither decreased platelet a ctivation (P-selectin(+) platelets) nor affected the number of platelet-leu kocyte aggregates (CD41(+) neutrophils) as measured by flow cytometry. Conclusion. Although NO may have inhibitory effects on platelet activation in vivo, our results confirm recent findings showing that NO donors were in effective in preventing platelet activation by extracorporeal circulation d uring cardiopulmonary bypass or plateletpheresis. Thus, NO donors do not ap pear to be ideal candidate drugs to inhibit HD-associated platelet activati on.