title: Effects of oxygen on exercise-induced increase of pulmonary arterial pressure in idiopathic pulmonary fibrosis.
abstract: BACKGROUND
  Idiopathic pulmonary fibrosis (IPF) is a severe disease with no known effective therapy. Patients with IPF may develop severe increase of pulmonary arterial pressure (PAP) on exercise, the mechanisms of which is not clearly identified.
  
  
  OBJECTIVE
  To determine whether oxygen may correct the increase of PAP developed during exercise in patients with IPF.
  
  
  METHODS
  We performed a prospective study on patients with IPF and no hypoxaemia at rest. The absence of pulmonary hypertension (PH) at rest was confirmed by echocardiography (systolic PAP <35 mmHg). Eight patients underwent echocardiography during exercise in air and with oxygen (to maintain saturation of at least 94%). Right ventricle-right atrium gradient and cardiac output were measured at rest, after each increment and at peak. We then compared the echocardiographic results obtained for air and oxygen.
  
  
  RESULTS
  All patients developed significant increase of SPAP on exercise (73 +/- 14 mmHg in air). Oxygen did not significantly improve SPAP on exercise (SPAP: 76 +/- 15 mmHg). Echocardiographic characteristics were similar between air and oxygen except for exercise tolerance in term of workload (p=0.045) and endurance (p=0.017). Resting pulmonary function tests did not predict the occurrence of increase of PAP on exercise.
  
  
  CONCLUSIONS
  Our results demonstrate that oxygen does not improve exercise-induced increase of PAP in patients with IPF and support the hypothesis that hypoxic vaso-constriction is not the main mechanism of acute increase of PAP during exercise.
authors.affiliation: Clinique des Maladies Respiratoires, Centre de Compétence Maladies Orphelines Pulmonaires, University Hospital, CHRU, Lille, France.
authors.forename: S
authors.initials: S
authors.lastname: Pouwels-Fry
authors.forename: S
authors.initials: S
authors.lastname: Pouwels
authors.forename: C
authors.initials: C
authors.lastname: Fournier
authors.forename: A
authors.initials: A
authors.lastname: Duchemin
authors.forename: I
authors.initials: I
authors.lastname: Tillie-Leblond
authors.forename: T
authors.initials: T
authors.lastname: Le Tourneau
authors.forename: B
authors.initials: B
authors.lastname: Wallaert
mesh_terms: D000368:Aged; D015150:Echocardiography, Doppler; D005081:Exercise Therapy / Q000009:adverse effects*; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D054990:Idiopathic Pulmonary Fibrosis / Q000378:metabolism / Q000503:physiopathology / Q000534:rehabilitation*; D008297:Male; D010101:Oxygen Consumption / Q000502:physiology*; D011379:Prognosis; D011446:Prospective Studies; D011669:Pulmonary Wedge Pressure / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology