title: Importance of hypoxic vasoconstriction in maintaining oxygenation during acute lung injury.
abstract: OBJECTIVE
  To investigate the role of hypoxic pulmonary vasoconstriction in the intrapulmonary blood flow redistribution and gas exchange protection during oleic acid acute lung injury.
  
  
  METHODS
  Prospective, controlled animal study.
  
  
  METHODS
  Research laboratory of an academic institution.
  
  
  METHODS
  Three groups of five mongrel dogs.
  
  
  METHODS
  Induction of acute lung injury by 0.08 mL/kg oleic acid intravenously. Hypoxic pulmonary vasoconstriction inhibition by Escherichia coli endotoxin microdose (15 microg/kg) pretreatment or by metabolic alkalosis (pH 7.60).
  
  
  RESULTS
  Pulmonary arterial and venous resistances were determined by flow-pressure curves and by capillary pressure estimation. Regional lung water and pulmonary blood flow were assessed by positron emission tomography. Oleic acid alone increased the arterial and venous resistances, redistributed blood flow away from edematous areas, and decreased the Pao2 from 507 +/- 16 to 373 +/- 60 torr. on Fio2 1.0 and positive end-expiratory pressure 5 cm H2O. Endotoxin pretreatment inhibited the increase in arterial resistance, suppressed the redistribution, and decreased the Pao2 to 105 +/- 22 torr. Alkalosis inhibited the increase in arterial and venous resistances, suppressed the redistribution, and decreased the Pao2 to 63 +/- 12 torr. Reversal of the alkalosis increased the arterial and venous resistances, restored the perfusion redistribution, and improved the Pao2 to 372 +/- 63 torr. Changes in blood gases conformed to predictions of a computer lung model in which hypoxic pulmonary vasoconstriction was suppressed by endotoxin and alkalosis.
  
  
  CONCLUSIONS
  We conclude that in oleic acid-induced lung injury, a) pulmonary hypertension results from increases in both arterial and venous resistances; b) the increase in arterial resistance is the primary mechanism responsible for the perfusion redistribution and the gas exchange protection; and c) the increase in arterial resistance is most consistent with hypoxic pulmonary vasoconstriction.
authors.affiliation: Washington University School of Medicine, St. Louis, MO, USA. sbrimi@ulb.ac.be
authors.forename: Serge
authors.initials: S
authors.lastname: Brimioulle
authors.forename: Valérie
authors.initials: V
authors.lastname: Julien
authors.forename: René
authors.initials: R
authors.lastname: Gust
authors.forename: James K
authors.initials: JK
authors.lastname: Kozlowski
authors.forename: Robert
authors.initials: R
authors.lastname: Naeije
authors.forename: Daniel P
authors.initials: DP
authors.lastname: Schuster
mesh_terms: D000818:Animals; D004285:Dogs; D006976:Hypertension, Pulmonary / Q000209:etiology; D000860:Hypoxia / Q000209:etiology; D019301:Oleic Acid; D011652:Pulmonary Circulation / Q000502:physiology*; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000503:physiopathology*; D014655:Vascular Resistance; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D019301:Oleic Acid