OBJECTIVES: Hypoxic pulmonary vasoconstriction is the primary physiologic mechanism that maintains a proper ventilation/perfusion match, but it fails in diffuse lung injuries such as acute respiratory distress syndrome. Acute respiratory distress syndrome is associated with pulmonary surfactant loss that alters alveolar mechanics (i.e., dynamic change in alveolar size and shape during ventilation), converting normal stable alveoli into unstable alveoli. We hypothesized that alveolar instability stents open pulmonary microvessels and is the mechanism of hypoxic pulmonary vasoconstriction failure associated with acute respiratory distress syndrome. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Ten adult pigs. INTERVENTIONS: Anesthetized ventilated pigs were prepared surgically for hemodynamic monitoring and were subjected to a right thoracotomy. An in vivo microscope was attached to the right lung, and the microvascular response to hypoxia (F(IO(2)), 15%) was measured in a lung with normal stable alveoli and in a lung with unstable alveoli caused by surfactant deactivation (Tween lavage). MEASUREMENTS AND MAIN RESULTS: Alveolar instability, defined as the difference between alveolar area at peak inspiration and end expiration and assessed as a percentage change (I-E Delta%), was significantly increased after Tween (23.9 +/- 3.0, I-E Delta%) compared with baseline (2.4 +/- 1.0, I-E Delta%). Alveolar instability was associated with the following microvascular changes: a) increased vasoconstriction (Tween, 14.9 +/- 1.0%) in response to hypoxia compared with baseline (10.8 +/- 1.2%, p <.05); and b) increased mean vascular diameter (Tween, 41.2 +/- 1.5 microm) compared with the mean diameter at baseline (24.6 +/- 1.0 microm, p <.05). CONCLUSION: Unstable alveoli stent open pulmonary vessels, which may explain the failure of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome.
OBJECTIVES:Hypoxic pulmonary vasoconstriction is the primary physiologic mechanism that maintains a proper ventilation/perfusion match, but it fails in diffuse lung injuries such as acute respiratory distress syndrome. Acute respiratory distress syndrome is associated with pulmonary surfactant loss that alters alveolar mechanics (i.e., dynamic change in alveolar size and shape during ventilation), converting normal stable alveoli into unstable alveoli. We hypothesized that alveolar instability stents open pulmonary microvessels and is the mechanism of hypoxic pulmonary vasoconstriction failure associated with acute respiratory distress syndrome. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Ten adult pigs. INTERVENTIONS: Anesthetized ventilated pigs were prepared surgically for hemodynamic monitoring and were subjected to a right thoracotomy. An in vivo microscope was attached to the right lung, and the microvascular response to hypoxia (F(IO(2)), 15%) was measured in a lung with normal stable alveoli and in a lung with unstable alveoli caused by surfactant deactivation (Tween lavage). MEASUREMENTS AND MAIN RESULTS: Alveolar instability, defined as the difference between alveolar area at peak inspiration and end expiration and assessed as a percentage change (I-E Delta%), was significantly increased after Tween (23.9 +/- 3.0, I-E Delta%) compared with baseline (2.4 +/- 1.0, I-E Delta%). Alveolar instability was associated with the following microvascular changes: a) increased vasoconstriction (Tween, 14.9 +/- 1.0%) in response to hypoxia compared with baseline (10.8 +/- 1.2%, p <.05); and b) increased mean vascular diameter (Tween, 41.2 +/- 1.5 microm) compared with the mean diameter at baseline (24.6 +/- 1.0 microm, p <.05). CONCLUSION: Unstable alveoli stent open pulmonary vessels, which may explain the failure of hypoxic pulmonary vasoconstriction in acute respiratory distress syndrome.