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Divisions of 1Cardiology and 2Haematology and Departments of 3Critical Care Medicine, 4Pediatrics, and 5Population Health Sciences, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada M5G 1X8
Submitted 19 July 2002 ; accepted in final form 2 May 2003
Effects of inhaled nitric oxide (NO) on human platelet function are controversial. It is uncertain whether intraplatelet cGMP mediates the effect of inhaled NO on platelet function. We investigated the effect of 30 ppm inhaled NO on platelet aggregation and plasma and intraplatelet cGMP in 12 subjects. We performed platelet aggregation studies by using a photooptical aggregometer and five agonists (ADP, collagen, epinephrine, arachidonic acid, and ristocetin). During inhalation, the maximal extent of platelet aggregation decreased by 75% with epinephrine (P < 0.005), 56% with collagen (P < 0.005), and 20% with arachidonic acid (P < 0.05). Responses to ADP (8% P > 0.05) and ristocetin (5% P > 0.05) were unaffected. Platelet aggregation velocity decreased by 64% with collagen (P < 0.005), 60% with epinephrine (P < 0.05), 33% with arachidonic acid (P < 0.05), and 14% with ADP (P > 0.05). Plasma cGMP levels increased from 2.58 ± 0.43 to 9.99 ± 5.57 pmol/ml (P < 0.005), intraplatelet cGMP levels were unchanged (means ± SD: 1.96 ± 0.58 vs. 2.71 ± 1.67 pmol/109 platelets; P > 0.05). Inhaled NO inhibits platelet aggregation via a cGMP independent mechanism.
nitric oxide; platelet aggregation; cGMP
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