Trial reportNitric oxide : biology and chemistry2020
Inhaled nitric oxide to control platelet hyper-reactivity in patients with acute submassive pulmonary embolism.
Trial report in Nitric oxide : biology and chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Safety and practicality of high dose inhaled nitric oxide in emergency department COVID-19 patients.The American journal of emergency medicine · 2022Trial
- Oxidative stress in acute pulmonary embolism: emerging roles and therapeutic implications.Thrombosis journal · 2024Review
- Mitochondrial Respiration of Platelets: Comparison of Isolation Methods.Biomedicines · 2021Article
- Thromboelastography Parameters and Platelet Count on Admission to the ICU and the Development of Venous Thromboembolism in Patients With Coronavirus Disease 2019.Critical care explorations · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundWe test if inhaled nitric oxide (NO) attenuates platelet functional and metabolic hyper-reactivity in subjects with submassive pulmonary embolism (PE).
methodsParticipants with PE were randomized to either 50 ppm NO + O2 or O2 only for 24 h with blood sampling at enrollment and after treatment; results were compared with healthy controls. Platelet metabolic activity was assessed by oxygen consumption (basal and uncoupled) and reactivity was assessed with agonist-stimulated thromboelastography (TEG) and fluorometric measurement of agonist-stimulated cytosolic [Ca
resultsParticipants (N = 38 per group) were well-matched at enrollment for PE severity, comorbidities as well as TEG parameters and platelet O2 consumption. NO treatment doubled the mean plasma [NO3-] (P < 0.001) indicating successful delivery, but placebo treatment produced no change. After 24 h, neither TEG nor O2 consumption parameters differed significantly between treatment groups. Platelet cytosolic [Ca
conclusionsIn patients with acute submassive PE, despite evidence of adequate drug delivery, inhaled NO had no major effect on platelet O2 consumption or agonist-stimulated parameters on TEG. Pharmacological activation, but not stimulation, of sGC effectively decreased platelet cytosolic [Ca
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Registered trials
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