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Title

Inhaled NO inhibits platelet aggregation and elevates plasma but not intraplatelet cGMP in healthy human volunteers

Authors
Sparling, Catherine
Cox, Peter N
Stephens, Derek
Adatia, Ian
Published in American Journal of Physiology. Heart and Circulatory Physiology. 2003, vol. 285, no. 2, p. H637-42
Abstract 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.
Keywords Administration, InhalationAdultBlood Platelets/drug effects/metabolismCyclic GMP/bloodFemaleHemoglobinsHumansMaleMiddle AgedNitric Oxide/administration & dosagePlatelet Aggregation/drug effectsPlatelet Count
Identifiers
PMID: 12750066
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Article (Published version) (106 Kb) - public document Free access
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Research group L'hypertension pulmonaire (pédiatrie) (228)
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BEGHETTI, Maurice et al. Inhaled NO inhibits platelet aggregation and elevates plasma but not intraplatelet cGMP in healthy human volunteers. In: American Journal of Physiology. Heart and Circulatory Physiology, 2003, vol. 285, n° 2, p. H637-42. https://archive-ouverte.unige.ch/unige:55333

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Deposited on : 2015-04-09

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