help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by PAPAZIAN, L.
Right arrow Articles by AUFFRAY, J.-P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by PAPAZIAN, L.
Right arrow Articles by AUFFRAY, J.-P.

Am. J. Respir. Crit. Care Med., Volume 160, Number 2, August 1999, 473-479

Inhaled Nitric Oxide and Vasoconstrictors in Acute Respiratory Distress Syndrome

LAURENT PAPAZIAN, ANTOINE ROCH, FABIENNE BREGEON, XAVIER THIRION, FRANÇOISE GAILLAT, PIERRE SAUX, VINCENT FULACHIER, YVES JAMMES, and JEAN-PIERRE AUFFRAY

Service de Réanimation, Service d'Information Médicale, Hôpital Sainte-Marguerite, Marseille; and Laboratoire de Physiopathologie, Faculté de Médecine de Marseille-Nord, Marseille, France

It has been suggested that the increase in PO2 observed with nitric oxide (NO) should be enhanced by the addition of a vasoconstrictor agent. The vasoconstrictor used in combination with NO should mimic or enhance hypoxic vasoconstriction. The aim of this study was to evaluate the respiratory and hemodynamic effects of norepinephrine (a nonspecific vasoconstrictor), almitrine bismesylate (a specific pulmonary vasoconstrictor), and inhaled NO, alone or together. During a 6-mo period, 16 patients presenting with ARDS were prospectively investigated. On inclusion, no patient was receiving cardiovasoactive drugs. The protocol consisted of seven consecutive phases: baseline, norepinephrine (in order to obtain a 3 mm Hg rise in mean pulmonary arterial pressure [<OVL>Ppa</OVL>]), almitrine bismesylate (16 µg/kg/min), inhaled NO (20 ppm delivered during inspiration), norepinephrine + inhaled NO, almitrine bismesylate + inhaled NO, almitrine bismesylate + norepinephrine + inhaled NO. General factorial analysis of variance showed that inhaled NO and almitrine bismesylate increased oxygenation (p < 0.0001). Norepinephrine had no effect on oxygenation. A synergistic effect between inhaled NO and almitrine bismesylate was found (p < 0.05), whereas norepinephrine did not affect the response to inhaled NO. Nitric oxide produced a significant decrease in <OVL>Ppa</OVL> and pulmonary vascular resistances (PVRI) (p < 0.0001). Both almitrine bismesylate and norepinephrine induced an increase in <OVL>Ppa</OVL> (p < 0.0001). Norepinephrine increased PVRI (p < 0.002), whereas almitrine bismesylate had no effect on PVRI. The present results support the hypothesis that a selective pulmonary vasoconstrictor enhances the increase in oxygenation induced by inhaled NO, whereas norepinephrine attenuates this effect.




This article has been cited by other articles:


Home page
 NEJMHome page
L. Chiche, J.-M. Forel, L. Papazian, Y. Asakura, T. Komatsu, T. Busch, S. Bercker, U. Kaisers, and A. Malhotra
Low-Tidal-Volume Ventilation
N. Engl. J. Med., December 13, 2007; 357(24): 2518 - 2520.
[Full Text] [PDF]

Home page
 ChestHome page
M. Maeder, T. Fehr, H. Rickli, and P. Ammann
Sepsis-Associated Myocardial Dysfunction: Diagnostic and Prognostic Impact of Cardiac Troponins and Natriuretic Peptides
Chest, May 1, 2006; 129(5): 1349 - 1366.
[Abstract] [Full Text] [PDF]

Home page
 Br J AnaesthHome page
G. M. Hermans, A. Wilmer, D. C. Knockaert, and H. Bobbaers
Acute intracardiac right-to-left shunt in a patient with acute respiratory distress syndrome and shock successfully treated with nitric oxide
Br. J. Anaesth., February 1, 2006; 96(2): 268 - 269.
[Full Text] [PDF]

Home page
 Br J AnaesthHome page
T. Silva-Costa-Gomes, L. Gallart, J. Valles, L. Trillo, J. Minguella, and M. M. Puig
Low- vs high-dose almitrine combined with nitric oxide to prevent hypoxia during open-chest one-lung ventilation
Br. J. Anaesth., September 1, 2005; 95(3): 410 - 416.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
N. Dalibon, M. Moutafis, N. Liu, J.-D. Law-Koune, S. Monsel, and M. Fischler
Treatment of Hypoxemia During One-Lung Ventilation Using Intravenous Almitrine
Anesth. Analg., March 1, 2004; 98(3): 590 - 594.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
L. G. Fischer, H. V. Aken, and H. Burkle
Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists
Anesth. Analg., June 1, 2003; 96(6): 1603 - 1616.
[Full Text] [PDF]

Home page
 Eur Respir JHome page
E.D. Moloney and T.W. Evans
Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome
Eur. Respir. J., April 1, 2003; 21(4): 720 - 727.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
R. T. Schermuly, A. Roehl, N. Weissmann, H. A. Ghofrani, H. Leuchte, F. Grimminger, W. Seeger, and D. Walmrath
Combination of nonspecific PDE inhibitors with inhaled prostacyclin in experimental pulmonary hypertension
Am J Physiol Lung Cell Mol Physiol, December 1, 2001; 281(6): L1361 - L1368.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 1999 American Thoracic Society 		  Solid Organ Transplant for the Intensivist 2008