Key result
Prolonged inhalation of nitric oxide at 30 p.p.m. increased bleeding time in healthy subjects, but caused only mild attenuation of platelet function compared to aspirin.
Why the study?
Does inhaled nitric oxide attenuate platelet function in vivo compared to aspirin in healthy subjects?
Does inhaled nitric oxide attenuate platelet function in vivo compared to aspirin in healthy subjects?
Inhaled nitric oxide causes only mild attenuation of platelet function in healthy subjects with normal endogenous nitric oxide production, unlike the pronounced effects of aspirin.
Answers are grounded in this paper and cite their sources.
May alter platelet function in healthy subjects; leaves open relevance to bleeding risk in patients.
Nitric oxide has platelet-stabilizing effects. Inhaled nitric oxide is used to treat pulmonary disorders, and may prolong bleeding times, suggesting that it has effects on haemostasis. We therefore examined if inhaled nitric oxide influences platelet function in vivo in healthy subjects. 2. Platelet aggregability (filtragometry ex vivo, which reflects aggregability in vivo), bleeding time and platelet secretion products and cGMP in plasma were studied during inhalation of two different doses of nitric oxide (30 and 80 p.p.m.; 15 min at each dose level; n = 19) and during prolonged (55 min; n = 18) inhalation of 30 p.p.m. nitric oxide. For comparison, studies were also performed before and after ingestion of 640 mg aspirin in 13 of the healthy subjects. 3. Plasma cGMP increased dose dependently during nitric oxide inhalation, suggesting guanylate cyclase activation in vivo. Platelet aggregability was, however, little affected and platelet secretion was not attenuated by nitric oxide inhalation. Bleeding time tended to increase (by 16-33%), but was significantly increased only after prolonged inhalation of nitric oxide at 30 p.p.m. 4. Aspirin (640 mg orally) caused pronounced and significant prolongations of filtragometry readings and bleeding time. Thus, the methods used were able to reveal platelet stabilization. 5. We conclude that nitric oxide inhalation causes only mild, if any, attenuation of platelet function in healthy subjects with a normal endogenous nitric oxide production. The effects may be different in disease states.
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Albert et al. (1996) studied Healthy subjects (n=19). Inhaled nitric oxide vs. Aspirin (640 mg orally) was evaluated on Platelet aggregability, bleeding time, platelet secretion products, and plasma cGMP. Prolonged inhalation of nitric oxide at 30 p.p.m. increased bleeding time in healthy subjects, but caused only mild attenuation of platelet function compared to aspirin.
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