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Alveolar mechanics alter hypoxic pulmonary vasoconstriction
Ulysse G McCann1, Henry J Schiller, Louis A Gatto
1SUNY Upstate Medical University, Department of Surgery, Syracuse, NY, USA.
Critical Care Medicine
|June 20, 2002
Summary
Alveolar instability in acute respiratory distress syndrome may cause pulmonary vessels to remain open, explaining the failure of hypoxic pulmonary vasoconstriction. This study used pigs to investigate this mechanism.
Area of Science:
- Pulmonary Physiology
- Respiratory Medicine
- Vascular Biology
Background:
- Hypoxic pulmonary vasoconstriction (HPV) is crucial for matching ventilation and perfusion.
- HPV fails in diffuse lung injuries like acute respiratory distress syndrome (ARDS).
- ARDS involves surfactant loss, leading to unstable alveoli and altered lung mechanics.
Purpose of the Study:
- To test the hypothesis that alveolar instability stents open pulmonary microvessels.
- To investigate if this stenting mechanism explains HPV failure in ARDS.
Main Methods:
- Prospective, randomized, controlled study in a university research laboratory.
- Ten adult pigs were surgically prepared for hemodynamic monitoring.
- In vivo microscopy assessed microvascular response to hypoxia in lungs with stable versus unstable alveoli (induced by surfactant deactivation).
Main Results:
- Alveolar instability (I-E Delta%) significantly increased after surfactant deactivation (23.9% vs. 2.4%).
- Hypoxia induced greater vasoconstriction in unstable alveoli (14.9% vs. 10.8%).
- Mean vascular diameter increased in unstable alveoli (41.2 µm vs. 24.6 µm).
Conclusions:
- Alveolar instability appears to stent pulmonary vessels open.
- This stenting may be the mechanism underlying HPV failure in acute respiratory distress syndrome.