Intrapulmonary blood flow redistribution during hypoxia increases gas exchange surface area

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Abstract
Airway hypoxia was previously shown to cause pulmonary capillary recruitment and raises diffusing capacity for CO2. Whether these events were caused by an increse in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung or by an increase in cardiac output was studied. Capillary recruitment at the top of the dog lung was measured by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for CO2 and blood flow distribution by radioactive microspheres. During airway hypoxia, recruitment occurred, diffusing capacity increased and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i.e., capillary derecruitment occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. Widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.