The development of the pulmonary arterial system follows a similar progression to that of the developing airways. Development of, and branching of the pulmonary artery mirrors bronchial branching, and later mirrors alveolar development. By the beginning of the cannalicular stage arteries in the pre acinar region have formed. The development of muscle within the wall of the pulmonary blood vessels lags behind structural development. Muscularization of intra-acinar arteries does not keep pace with the appearance of new arteries and is not complete until childhood. What is the significance of this? Although the control of the pulmonary blood flow in terms of distribution within the lung is controlled by a number of factors (physical location of lung units, gravity, oxygen, nitric oxide), alveolar oxygen tension is probably the most important determinant of pulmonary blood flow. The ultimate effector governing the distribution of pulmonary blood flow is pulmonary vascular muscle. The process of hypoxic pulmonary vasoconstriction governs this distribution of blood flow. Decreased alveolar oxygen tension will caused vasoconstriction in the area of the alveolus with a decreased oxygen tension, thus diverting blood to better oxygenated areas of the lung. During a generalized decrease in oxygen tension, or hypoxia, there is vasoconstriction of pulmonary blood vessels throughout the lung which causes a rise in pulmonary artery pressure.
Why is there is so little blood flow in pulmonary artery in the fetus, and why does this suddenly change with the first breath after birth? The fetal alveolus is filled with liquid not exposed to the atmosphere, therefore oxygen tension in the alveolus is very low. As a consequence of this low oxygen tension in the alveolus, there is generalized pulmonary vasoconstriction, arise in pulmonary artery pressure, and diversion of blood flow from the pulmonary bed, across the ductus arteriosus to the systemic circulation. At birth, as the alveoli become gas filled, and oxygen tension in the alveolus rises, vasoconstriction decreases, and blood flow now increases to the lung. The mediator of the vasodilatation in the pulmonary bed is nitric oxide. Pulmonary artery pressure is decreases after birth. In a small number of neonatus the nitric oxide system in the pulmonary vascular bed is dysfunctional and pulmonary arterial vasodilatation does not occur after birth. When this is occurs pulmonary artery pressure remain elevated, the ductus arteriosus remain open, blood with low oxygen tension is shunted into the systemic circulation (a situation analogous to that found in the fetus) and systemic oxygen delivery is compromised. This syndrome, originally called persistent fetal circulation, is now called persistent pulmonary hypertension of the newborn.