Intrapulmonary arteriovenous anastomoses. Physiological, pathophysiological, or both?

Large-diameter, intrapulmonary arteriovenous anastomoses exist in human lungs. In developing fetuses, blood flows physiologically through pulmonary arteriovenous channels that appear to regress during lung maturation. Blood flow through intrapulmonary arteriovenous anastomoses is a normal occurrence during exercise or inhalation of reduced oxygen gas mixtures in most healthy humans. However, the importance of blood flow through these anastomoses to the efficiency of pulmonary gas exchange in normal and pathological states remains controversial. Newly reported three-dimensional dissections of human lung samples provide direct anatomic evidence of intrapulmonary arteriovenous anastomoses in the lungs of prematurely born infants, and suggest that these vessels contribute consequentially to the severe arterial hypoxemia experienced by infants who die of bronchopulmonary dysplasia. Surgical construction of a cavopulmonary anastomosis can also induce pathological arteriovenous shunting suggestive of a regression to the fetal state, possibly implicating an enigmatic hepatic factor in arteriovenous shunt regulation. These two observations support an important contribution of blood flow through intrapulmonary arteriovenous anastomoses to arterial hypoxemia under at least some pathological conditions. The degree to which these vessels contribute to arterial hypoxemia in other disease states where intrapulmonary shunting is present, such as hepatopulmonary syndrome, remains unknown.