Inhaled nitric oxide does not enhance lipid peroxidation in patients with acute respiratory distress syndrome

• Verfasst von: Weigand, Markus A. [VerfasserIn]
• Verfasst von: Snyder-Ramos, Stephanie [VerfasserIn]
• Verfasst von: Möllers, Andrea [VerfasserIn]
• Verfasst von: Bauer, Jens [VerfasserIn]
• Verfasst von: Hansen, Dirk [VerfasserIn]
• Verfasst von: Kochen, Walter [VerfasserIn]
• Verfasst von: Martin, Eike [VerfasserIn]
• Verfasst von: Motsch, Johann [VerfasserIn]
• Titel: Inhaled nitric oxide does not enhance lipid peroxidation in patients with acute respiratory distress syndrome
• Verf.angabe: Markus A. Weigand, MD; Stephanie A. Snyder-Ramos, MD; Andrea G. Möllers, PhD; Jens Bauer, MD; Dirk Hansen, PhD; Walter Kochen, PhD; Eike Martin, MD, FANZCA; Johann Motsch, MD
• E-Jahr: 2000
• Jahr: 2000/10/01
• Umfang: 7 S.
• Fussnoten: Gesehen am 01.12.2017
• Titel Quelle: Enthalten in: Critical care medicine
• Ort Quelle: Hagerstown, Md. : Lippincott Williams & Wilkins, 1973
• Jahr Quelle: 2000
• Band/Heft Quelle: 28(2000), 10, Seite 3429-3435
• ISSN Quelle: 1530-0293
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Dose-Response Relationship, Drug
• Sach-SW: Humans
• Sach-SW: Female
• Sach-SW: Male
• Sach-SW: Middle Aged
• Sach-SW: Time Factors
• Sach-SW: Nitric Oxide
• Sach-SW: Aged
• Sach-SW: Prospective Studies
• Sach-SW: Administration, Inhalation
• Sach-SW: Aldehydes
• Sach-SW: Bronchodilator Agents
• Sach-SW: Drug Monitoring
• Sach-SW: Free Radical Scavengers
• Sach-SW: Lipid Peroxidation
• Sach-SW: Malondialdehyde
• Sach-SW: Respiratory Distress Syndrome, Adult
• Sach-SW: Survival Analysis
• Sach-SW: Treatment Outcome
• K10plus-PPN: 1565951204

Abstract

OBJECTIVE: To investigate whether inhaled nitric oxide (NO) enhances pulmonary lipid peroxidation as indicated by arterial blood levels of malondialdehyde, hexanal, and pentanal in patients with acute respiratory distress syndrome (ARDS). DESIGN: Prospective, nonrandomized, controlled trial. SETTING: Surgical intensive care unit in a university hospital. PATIENTS: Twenty-five patients with ARDS, as defined by the American-European Consensus Conference, and a PaO2/FIO2 < or = 170 mm Hg were enrolled in the study. Four healthy subjects were studied as controls. INTERVENTIONS: On enrollment of the patients in the study, a dose-response test with increasing concentrations of inhaled NO (0, 2, 10, 40, 0 ppm) was performed. Patients who showed an increase of >20% in PaO2 were designated as responders and all others as nonresponders. In responders, this dose-response test was followed by 24 hrs of continuous treatment with inhaled NO at the best NO concentration determined during the dose-response test, whereas nonresponders received standard care. For healthy volunteers, the dose-response test took the form of spontaneous breathing of the same NO concentrations. MEASUREMENTS AND MAIN RESULTS: Eighteen patients (72%) showed an increase of >20% in PaO2 during the dose-response test. This significant improvement in arterial oxygenation in responders led to a significant reduction in FIO2 (responders, 0.73 +/- 0.05 vs. nonresponders, 0.89 +/- 0.05) after 24 hrs of therapy. On enrollment, arterial blood concentrations of malondialdehyde, hexanal, and pentanal were significantly higher than those of healthy volunteers. In addition, arterial concentrations of hexanal and pentanal exceeded mixed venous levels two- to ten-fold. Inhalation of NO did not significantly alter these blood concentrations either during the dose response test or during 24 hrs of therapy. CONCLUSIONS: In patients with ARDS, malondialdehyde, hexanal, and pentanal were significantly elevated, indicating lipid peroxidation. Lipid peroxidation was not further affected by inhalation of NO.