Inhibition of Platelet Aggregation by Inhaled Nitric Oxide in Patients with Acute Respiratory Distress Syndrome

Samama, Ch.M.; Diaby, M.; Mdhafar, Ayoub; Eyraud, Daniel; Arock, Michel; Guillosson, Jean‐Jacques; Coriat, Pierre; Rouby, Jean-Jacques

doi:10.1097/00132586-199610000-00020

Cited by 39 publications

(48 citation statements)

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“…The maximal inhibition of platelet aggregation was already achieved at 3 ppm NO during inhalation of 1 to 100 ppm NO in a comparable study population. 10 In healthy volunteers inhaling 30 ppm NO, no further prolongation of bleeding time was observed at 80 ppm. 28 In comparison with these studies, no definitive dose-related effect of inhaled NO on platelet function could be found in animals, 8,11 and further studies are necessary to investigate a dose relation in a larger study population.…”

Section: Discussionmentioning

confidence: 96%

“…36 Recently, it was shown that 3 to 30 ppm inhaled NO inhibits platelet aggregation without prolonging bleeding time in patients with ARDS. 10 In addition, platelet activation was abolished during NO administration in pigs after acute pulmonary embolism. 11 In accordance with our findings, most of these studies demonstrated inhaled NO to have an inhibitory effect on platelet function.…”

Section: Discussionmentioning

confidence: 96%

“…32 When collagen was used to induce platelet aggregation, however, this inhibition was observed later and to a lesser extent, as also reported by other investigators. 10,33,34 This may be explained by the relatively high collagen concentration that was used in the aggregation studies. Lower concentrations of collagen or the use of epinephrine, which led to good results in the in vitro bleeding time measurements, might have revealed a comparable platelet inhibitory effect.…”

Section: Discussionmentioning

confidence: 99%

“…11 In accordance with our findings, most of these studies demonstrated inhaled NO to have an inhibitory effect on platelet function. Different findings with regard to bleeding time and platelet aggregation may be explained by the different methods and study populations that were used 10,11,18,23,28 and are therefore not necessarily contradictory.…”

Section: Discussionmentioning

confidence: 99%

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Inhaled Nitric Oxide Inhibits Human Platelet Aggregation, P-Selectin Expression, and Fibrinogen Binding In Vitro and In Vivo

et al. 1998

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Inhaled Nitric Oxide Inhibits Human Platelet Aggregation, P-Selectin Expression, and Fibrinogen Binding In Vitro and In Vivo

et al. 1998

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“…In the present study, NO concentrations delivered to the patient were determined by sampling the endotracheal gas using a fast response chemiluminescence apparatus in order to accurately measure inspiratory NO concentration [9]. If used, slow response chemiluminescence would have underestimated the true inspiratory NO concentration by averaging it together with the expiratory level, as probably occurred in two of our previous studies [4,23]. Another reason for determining the inspiratory NO concentration in this way was the method of NO administration used.…”

Section: Discussionmentioning

confidence: 99%

Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose–response study

et al. 1997

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Background: The aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). Results: Eight patients with ARDS and without septic shock (PaO 2 = 95 ± 16 mmHg, PEEP = 0, FiO 2 = 1.0), and eight patients with ARDS and septic shock (PaO 2 = 88 ± 11 mmHg, PEEP = 0, FiO 2 = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO 2 of at least 40 mmHg, at FiO 2 1.0 and PEEP 10 cmH 2 O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups, NO induced a dose-dependent decrease in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance index (PVRI), and venous admixture (Q VA /Q T ), and a dosedependent increase in PaO 2 /FiO 2 (P ≤ 0.012). Dose-response of MPAP and PVRI were similar in both groups with a plateau effect at 4.5 ppm. Dose-response of PaO 2 /FiO 2 was influenced by the presence of septic shock. No plateau effect was observed in patients with septic shock and PaO 2 /FiO 2 increased by 173 ± 37% at 150 ppm. In patients without septic shock, an 82 ± 26% increase in PaO 2 / FiO 2 was observed with a plateau effect obtained at 15 ppm. In both groups, dose-response curves demonstrated a marked interindividual variability and in five patients pulmonary vascular effect and improvement in arterial oxygenation were dissociated. Conclusion: For similar NOinduced decreases in MPAP and PVRI in both groups, the increase in arterial oxygenation was more marked in patients with septic shock.

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Inhaled nitric oxide for respiratory failure in preterm infants

Barrington

Finer

Pennaforte

2017

Cochrane Database of Systematic Reviews

153

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Background Inhaled nitric oxide (iNO) is e ective in term infants with hypoxic respiratory failure. The pathophysiology of respiratory failure and the potential risks of iNO di er substantially in preterm infants, necessitating specific study in this population. Objectives To determine e ects of treatment with inhaled nitric oxide (iNO) on death, bronchopulmonary dysplasia (BPD), intraventricular haemorrhage (IVH) or other serious brain injury and on adverse long-term neurodevelopmental outcomes in preterm newborn infants with hypoxic respiratory failure. Owing to substantial variation in study eligibility criteria, which decreases the utility of an overall analysis, we divided participants post hoc into three groups: (1) infants treated over the first three days of life because of defects in oxygenation, (2) preterm infants with evidence of pulmonary disease treated routinely with iNO and (3) infants treated later (a er three days of age) because of elevated risk of BPD. Search methods We used standard methods of the Cochrane Neonatal Review Group. We searched MEDLINE, Embase, Healthstar and the Cochrane Central Register of Controlled Trials in the Cochrane Library through January 2016. We also searched the abstracts of the Pediatric Academic Societies. Selection criteria Eligible for inclusion were randomised and quasi-randomised studies in preterm infants with respiratory disease that compared e ects of iNO gas versus control, with or without placebo. Data collection and analysis We used standard methods of the Cochrane Neonatal Review Group and applied the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach to assess the quality of evidence.

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Inhibition of Platelet Aggregation by Inhaled Nitric Oxide in Patients with Acute Respiratory Distress Syndrome

Cited by 39 publications

References 0 publications

Inhaled Nitric Oxide Inhibits Human Platelet Aggregation, P-Selectin Expression, and Fibrinogen Binding In Vitro and In Vivo

Inhaled Nitric Oxide Inhibits Human Platelet Aggregation, P-Selectin Expression, and Fibrinogen Binding In Vitro and In Vivo

Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose–response study

Inhaled nitric oxide for respiratory failure in preterm infants

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