Literature DB >> 15891329

Lack of alteration of endogenous nitric oxide pathway during prolonged nitric oxide inhalation in intensive care unit patients.

Anne-Claire Lukaszewicz1, Alexandre Mebazaa, Jacques Callebert, Joaquim Matéo, Claire Gatecel, Hakim Kechiche, Geneviève Maistre, Alain Carayon, Bruno Baudin, Didier Payen.   

Abstract

OBJECTIVE: To compare hemodynamic and gasometric variables and the plasma concentrations of nitric oxide metabolites (cyclic guanosine monophosphate and nitrate and nitrite), endothelin-1, and renin-angiotensin metabolites before and after the start of nitric oxide inhalation, after prolonged nitric oxide inhalation, and before and after nitric oxide withdrawal.
DESIGN: Prospective study.
SETTING: Surgical intensive care unit, university hospital.
SUBJECTS: Patients with acute lung injury and right ventricular failure.
INTERVENTIONS: Nitric oxide inhalation (10-12 ppm) during a median of 2.9 days (12 hrs to 6.5 days).
MEASUREMENTS AND MAIN RESULTS: The pulmonary vasodilator effects of inhaled nitric oxide improved arterial oxygenation in patients with acute lung injury (p < .05) and reduced right atrial pressure in patients with right ventricular dysfunction (p < .01). These beneficial effects lasted the whole period of prolonged inhaled nitric oxide therapy up to 6.5 days. However, when inhaled nitric oxide was withdrawn, pulmonary vasodilator effects rapidly disappeared, and Pao2/Fio2 ratio markedly deteriorated in all studied patients to return to pre-inhaled nitric oxide levels. Changes in plasma cyclic guanosine monophosphate and nitrate and nitrite paralleled those of pulmonary vasodilatory effects. An immediate increase in plasma cyclic guanosine monophosphate with a slightly delayed increase in plasma nitrate and nitrite was observed at inhaled nitric oxide start with no attenuation during the prolonged inhaled nitric oxide therapy. A marked decrease toward pre-inhaled nitric oxide levels was seen within hours of inhaled nitric oxide withdrawal. In addition, no alteration of plasma endothelin-1 or renin-angiotensin mediators was observed during or after inhaled nitric oxide therapy.
CONCLUSIONS: Our study showed a lack of attenuation in the beneficial effects of inhaled nitric oxide and a lack of alteration of endogenous nitric oxide, endothelin-1, and renin-angiotensin pathways during prolonged nitric oxide inhalation.

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Year:  2005        PMID: 15891329     DOI: 10.1097/01.ccm.0000163233.00458.dd

Source DB:  PubMed          Journal:  Crit Care Med        ISSN: 0090-3493            Impact factor:   7.598


  3 in total

1.  Inhaled nitric oxide increases urinary nitric oxide metabolites and cyclic guanosine monophosphate in premature infants: relationship to pulmonary outcome.

Authors:  Philip L Ballard; Roberta L Keller; Dennis M Black; David J Durand; Jeffrey D Merrill; Eric C Eichenwald; William E Truog; Mark C Mammel; Robin Steinhorn; Rita M Ryan; Sherry E Courtney; Hart Horneman; Roberta A Ballard
Journal:  Am J Perinatol       Date:  2014-06-26       Impact factor: 1.862

2.  Endotoxin-induced myocardial dysfunction in senescent rats.

Authors:  Sandrine Rozenberg; Sophie Besse; Hélène Brisson; Elsa Jozefowicz; Abdelmejid Kandoussi; Alexandre Mebazaa; Bruno Riou; Benoît Vallet; Benoît Tavernier
Journal:  Crit Care       Date:  2006       Impact factor: 9.097

Review 3.  Inhaled nitric oxide therapy and risk of renal dysfunction: a systematic review and meta-analysis of randomized trials.

Authors:  Sheng-Yuan Ruan; Tao-Min Huang; Hon-Yen Wu; Huey-Dong Wu; Chong-Jen Yu; Mei-Shu Lai
Journal:  Crit Care       Date:  2015-04-03       Impact factor: 9.097

  3 in total

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